碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘过量对NOD和Balb/c鼠甲状腺TRAIL和TRAIL-sR1表达的影响

Objective To investigate the influence of iodine excess on expression of TRAIl/TRAIL-sR1 in NOD and Balb/c mice and to study the effect of TRAIl/TRAIL-sR1 on the pathogenesis of experimental autoimmune thyroiditis(EAT). Methods Both Balb/c and NOD mice were divided randomly into control and iodine excess group by feeding with water containing no NaI or 0.05% Nal. The mice were sacrificed after 8 weeks. TRAIL and TRAIL-sR1 mRNA levels were detected by RT-PCR. The function, morphology and apoptosis of thyroids were also observed by ELISA and Tunnel stain. Results Treated by HI, enlarged follicles and flattened epithelium by accumulation of colloid were found in thyroids of both NOD and Balb/c mice. But significant lymphoid cell infiltration and local fibrosis were only found in thyroids of NOD HI group. The relative weight of thyroids of NOD mice in HI group[(104.8±14.5)mg/kg]was heavier than that of control group [(71.8±20.4)mg/kg]. The level of TT4 declined in HI group[(30.77±3.59)mmol/L]compared with control group[(36.43±2.66)mmol/L], meanwhile, the level of TSH was higher in HI group[(6.98±0.66)μg/L]than that in control group [(5.55±0.56)μg/L]. The difference being statistically significant(t=7.773,-9.526,-4.458, all P < 0.05). The relative weight of thyroids of Balb/c mice of HI group[(155.8±20.8)mg/kg]also heavier than that of control group [(105.1±22.0) mg/kg]. The level of TT4 droped in HI group [(19.75±3.32) mmoL/L]was higher than that in control group[(23.46±6.21)mmoL/L], the level of TSH in HI group[(4.14±1.71)μg/L]was higher than that in control group[(3.55±1.41)μg/L], the difference being statistically significant(t=7.554,-7.239,3.140, all P< 0.05). A great deal of apoptotie ceils observed in NOD (3.97±0.91) and Balb/c mice (1.05±0.45) by Tunnel stain were greater than control groups (0.21±0.15, 0.10±0.03), the difference being statistically significant in beth of the two species(t=-7.167,-17.772, both P < 0.05). The apoptosis index of thyroid follicular epithelium in NOD was obviously higher than Balb/c(t=-7.625, P<0.05). The level of TRAIL mRNA did not remarkably change in Balb/c between control group(0.000 59±0.000 39) and HI group(0.001 24±0.000 46, t=-1.940, P>0.05), but it increased apparently in NOD mice HI group(0.018 88±0.005 77) than that of control group(0.009 61± 0.00591, t=-2.71, P<0.05). The level of the expression of TRAIL-sR1 mRNA increased in HI groups of NOD (0.000 53±0.000 15) and Balb/c mice(0.000 42±0.000 09) than that in control groups of NOD(0.000 28± 0.000 05) and Balb/c mice (0.000 17±0.000 06) and the differences were statistically significant between the two species(t=3.050,3.990, all P<0.05). The differences of the expression of TRAIL and TRAIL-sR1 mRNA between the two species were significant(t=-3.37,-4.76, all P<0.05). Conclusions Iodine excess induces colloid goiter in beth species of mice and thyroiditis in NOD mice. The increase of TRAIL and TRAIL-sR1 influenced by iodine excess is one of the molecular bases of follicular epithelium apoptosis and inflammation in thyroids. Genetic factor is a key factor in the pathogenesis of thyroiditis.     

碘诱发NOD和Balb/c小鼠甲状腺炎的实验研究

目的 观察碘过量对不同遗传背景小鼠甲状腺炎诱发作用的异同.方法 选用NOD和Balb/c小鼠各14只,每个品系小鼠均分为对照组、碘化钠(NaI)组,分别饮用纯净水和0.05%NaI水8周.放射免疫法(RIA)和ELISA法分别检测血清中总T4(TT4)、甲状腺球蛋白抗体(TgAb)、甲状腺过氧化物酶抗体(TPOAb)和促甲状腺激素(TSH)水平,光镜下观察甲状腺形态学改变和免疫组化染色的甲状腺细胞凋亡情况,四甲基偶氮唑兰(MTT)法检测颈部淋巴结和脾淋巴细胞对甲状腺球蛋白刺激的增殖反应.结果 饮碘水8周后,NOD和Balb/c小鼠甲状腺相对质量,NaI组[(104.83±14.52)、(155.79±20.77)mg/kg]较对照组[(71.80±20.42)、(105.15±21.98)mg/kg]明显增加(t值分别为-3.293、-4.429,P均<0.01),甲状腺组织表现为滤泡扩张、胶质潴留;NOD、Balb/c小鼠血清TT4水平,NaI组[(29.52±4.42)、(19.53±2.35)nmol/L]较对照组[(33.40±5.38)、(23.47±6.22)nmol/L]呈下降趋势(t值分别为1.374、1.567,P>0.05);血清TSH水平,与对照组[(3.55±1.41)、(5.55±0.56)μg/L]比较,Balb/c小鼠NaI组[(4.14±1.71)μg/L]呈升高趋势(t=-0.705,P>0.05),NOD小鼠NaI组[(6.98±0.66)μg/L]明显升高(t=-3.562,P<0.01);NOD、Balb/c小鼠NaI组TgAb(1281、1364 cpm)和TPOAb水平(2.50×103、0.14×103U/L)与对照组(1297、1220 cpm,3.17×103、0.03×103 U/L)比较没有明显变化(Z值分别为-0.081、-0.703,-0.244、-1.293,P均>0.05).NOD小鼠NaI组甲状腺细胞凋亡数量较BMb/c小鼠增加,并且甲状腺内可见大量淋巴细胞浸润,组织结构破坏和纤维化的灶性病变;NOD小鼠淋巴结和脾淋巴细胞数量,NaI组(1.100±0.014、1.076±0.033)较对照组(0.993±0.011、1.005±0.003)增加(t值分别为-11.672、-4.314,P均<0.01).结论 碘可致Balb/c鼠甲状腺肿大,功能下降;NOD鼠除七述病变外,甲状腺发生明显炎症反应,并且针对Tg产生了致敏的淋巴细胞.碘过量可诱发NOD鼠发生自身免疫性甲状腺炎.     

不同碘营养水平对哺乳期大鼠甲状腺和乳腺胰岛素样生长因子Ⅰ mRNA表达的影响

目的 观察不同碘营养水平对哺乳期大鼠甲状腺和乳腺胰岛素样生长因子Ⅰ(IGF-1)mRNA表达水平的影响.方法 30只雌性断乳1个月Wistar大鼠按体质量随机分成3组:低碘组、适碘组、高碘组,每组10只,食用合成饲料,分别饮用含碘0、150、3000 μg/L的去离子水.喂养3个月后,与雄鼠合笼交配,待母鼠哺乳5 d后将其处死、取母鼠乳腺、甲状腺及血清,温和酸消化法测定血清碘,放射免疫分析法测定T3、T4水平,实时荧光定量PCR法检测乳腺和甲状腺IGF-1 mRNA表达水平.结果 低碘组血清碘[(17.38±3.27)μg/L]低于适碘组[(43.42±6.92)μg/L,P<0.05],高碘组血清碘[(350.10±38.46)μg/L]高于适碘组(P<0.05);低碘组、高碘组T3水平[(1.11μ0.25)、(1.61±0.33)μg/L]低于适碘组[(2.18±0.46)μg/L,P均<0.05];低碘组、高碘组T4水平[(33.40±11.11)、(56.54±10.38)μg/L]与适碘组[(44.02±12.51)μg/L]比较差异无统计学意义(P>0.05),低碘组T4水平低于高碘组(P均<0.05);低碘组、高碘组甲状腺IGF-1 mRNA表达水平(0.34±0.08、0.23±0.08)均高于适碘组(0.15±0.03,P均<0.05);低碘组哺乳期乳腺IGF-1 mRNA表达水平(0.59±0.18)高于适碘组(0.40±0.10,P<0.05);3组甲状腺IGF-1 mRNA表达均低于同组的乳腺表达水平(t=3.54、6.44、2.62,P均<0.05).结论 碘能够影响哺乳期甲状腺和乳腺IGF-1 mRNA的表达,且哺乳期乳腺表达强于甲状腺.     

不同碘营养水平对哺乳期大鼠甲状腺和乳腺钠碘转运体mRNA表达的影响

目的 观察不同碘营养水平对哺乳期大鼠甲状腺和乳腺钠碘转运体(NIS)mRNA表达水平的影响.方法 Wistar大鼠30只,体质量40～60 g.按体质量将大鼠随机分成3组:低碘组(去离子水),适碘组(含碘150 μg/L的去离子水),高碘组(含碘3000μg/L的去离子水),3组均喂合成饲料.喂养3个月后,与雄鼠合笼交配,待母鼠哺乳5 d后处死,取母鼠乳腺、甲状腺及血清.采用温和酸消化法测定血清碘,放射免疫分析法测定血清T_3、T_4水平,实时荧光定量PCR法检测乳腺和甲状腺NIS mRNA表达.结果 哺乳期大鼠血清碘、T_3、T_4、NIS mRNA表达,组间比较差异有统计学意义(F值分别为499.94、16.67、8.49,H=7.58,P均<0.05).血清碘适碘组[(43.42±692)μg/L]高于低碘组[(17.38±3.27)μg/L,P<0.05],高碘组[(350.10±38.46)μg/L]高于适碘组(P<0.05).血清T_3水平,低碘组、高碘组[(1.11±0.25)、(1.61±0.33)μg/L]低于适碘组[(2.18±0.46)μg/L,P均<0.05].血清T_4水平,低碘组[(33.40±11.11)μg/L]低于高碘组[(56.54±10.38)μg/L,P<0.05].甲状腺NIS mRNA表达水平低碘组(0.280±0.030)高于适碘组(0.240±0.030,P<0.05).高碘组(0.069±0.037)低于适碘组(P<0.05).哺乳期乳腺NIS mRNA表达水平高碘组(0.027±0.007)低于适碘组(0.051±0.019,P<0.05).结论 轻度低碘能够提高甲状腺NIS mRNA表达,保护母体免受低碘的危害,但对下一代的保护作用不明显或没有保护作用;高碘抑制甲状腺和乳腺NIS mRNA表达,保护母体及下一代免受高碘的危害.     

碘缺乏和碘过量对实验性甲状腺功能减退小鼠血脂代谢的影响

目的 观察碘缺乏和碘过量对实验性甲状腺功能减退(简称甲减)小鼠血脂代谢的影响,探讨碘不依赖于甲状腺激素的独立作用机制.方法 将雌性Balb/c小鼠按体质量随机分为6组:对照、重度低碘(SID)、轻度低碘(MID)、适碘(NI)、10倍碘过量(10HI)和50倍碘过量(50HI)组,每组10只.对照组饲以低碘饲料,其他各组饲以含0.2%甲基硫氧嘧啶的低碘饲料,同时饮用碘化钾(KI)配制的含碘量分别为326.79、0、196.08、326.79、3856.21、19 542.50 μg/L的去离子水.喂养3个月后,处死并收集小鼠外周血,分离血清.放射免疫分析法测定甲状腺激素水平,酶法检测血清中甘油三酯(TG)、总胆固醇(TC)、高密度脂蛋白胆固醇(HDL-C)及低密度脂蛋白胆固醇(LDL-C)水平.结果 ①SID[(21.27±9.63)μg/L]、MID[(23.41±3.93)μg/L]、NI[(22.57±4.66)μg/L]、10HI[(21.07±5.03)μg/L]和50HI组[(21.46±5.90)μg/L]血清TT4水平明显低于对照组[(42.15±8.26)μg/L,P均＜0.01],而各组间血清TT3水平比较,差异无统计学意义(F=0.99,P＞0.05).②10HI组TG水平[(1.17±0.16)mmol/L]与对照组[(1.39±0.22)mmol/L]和NI组[(1.51±0.22)mmol/L]比较,明显降低(P均＜0.05).50HI组TG和TC水平[(1.18±0.22)、(1.78±0.15)mmol/L]与对照组[(1.39±0.22)、(2.14±0.37)mmol/L]和NI组[(1.51±0.22)、(2.00±0.15)mmol/L]比较,明显降低(P均＜0.05).各组HDL-C、LDL-C水平比较,差异无统计学意义(F值分别为0.55、0.54,P均＞0.05).结论 碘可不依赖于甲状腺激素独立发挥调节甲减小鼠血脂的作用;监控碘的摄入量,对有效防治心血管疾病亦有重要作用.

Abstract：

Objective To observe the effects of iodine deficiency and iodine excess on the lipid metabolism in an experimental hypothyroid model of mice and to explore the roles of iodine independent of its role in thyroid hormones. Methods Female Balb/c mice were randomly divided into 6 groups: control, severe iodine deficiency (SID), mild iodine deficiency(MID), normal iodine (NI), 10-fold high iodine (10HI) and 50-fold high iodine(50HI), 10 in each group. The mice in control group were fed with low iodine forage, other mice were fed with low iodine forage containing 0.2% methylthiouracilum. All mice drank deionic water containing different concentrations of potassium iodide(KI). The iodine content in water was 326.79, 0, 196.08,326.79, 385621, 19 542.50 μg/L, respectively. After three months, thyroid hormones in the serum were determined by radioimmunoassay.Also, the blood samples were analyzed for total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesteiol (HDL-C) and low density lipoprotein cholesterol (LDL-C) and measured enzymatically by automatic analyzer. Results ①The levels of Tr4 in SID[(21.27 ± 9.63)μg/L], MID[(23.41 ± 3.93)μg/L], NI[(22.57 ±4.66)μg/L], 10HI [(21.07 ± 5.03) μg/L] and 50HI groups [(21.46 ± 5.90) μg/L] were distinctively decreased compared with control group[(42.15 ± 8.26)μg/L, all P ＜ 0.01]. There were no statistical significant differences of TT3 between different groups (F = 0.99, P > 0.05 ). ②The level of TG in 10HI group [ ( 1.17 ± 0.16)mmol/L ] was obviously decreased compared with control [(1.39 ± 0.22 )mmol/L] and NI groups[(151 ± 0.22)mmol/L, all P＜ 0.05].Both TG and TC in 50HI group[(1.18 ± 0.22), (1.78 ± 0.15)mmol/L] were significantly decreased compared with control [( 1.39 ± 0.22), (2.14 ± 0.37)mmol/L] and NI groups [(1.51 ± 0.22), (2.00 ± 0.15)mmol/L, all P ＜ 0.05].The difference of serum HDL-C and LDL-C between the groups was not significant(F = 0.55,0.54, all P ＞ 0.05 ).Conclusions Dietary iodine plays a role in the metabolism of serum lipids independent of thyroid hormones.Thus, monitoring the amount of iodine intake during sodium restriction should also be taken extremely important for effectively prevention and cure of cardiovascular disease.     

碘过量和多聚肌苷酸-聚胞苷酸及甲状腺球蛋白诱发小鼠甲状腺炎对Toll样受体3表达的影响

目的 观察碘过量(high iodine,HI)和多聚肌苷酸-聚胞苷酸[Polyinosinic-Polycytidylic acid,Poly (I:C),Poly]及甲状腺球蛋白(Thyroglobulin,TG)诱发小鼠甲状腺炎对Toll样受体3(Toll-like receptor 3,TLR3)表达的影响,探讨TLR3在自身免疫性甲状腺炎发病中的作用.方法 NOD(Non-obese diabetic)小鼠42只,体质量(20±3)g.按体质量将小鼠随机分为6组:对照组、HI组、Poly组、TG组、HI+TG组、HI+Poly组,每组7只.对照组:饮用去离子水,腹腔注射生理盐水0.1 ml,每天1次,连续1周,在处死小鼠前1周隔日1次,同样剂量生理盐水再注射3次;HI组:饮用0.05%的碘化钠去离子水,腹腔注射生理盐水(同对照组);Poly 组:饮用去离子水,腹腔注射0.1 ml Poly(1 g/L,按5 mg/kg体质量),每天1次,连续1周,处死前1周隔日1次,同剂量Poly再注射3次;TG组:饮去离子水,腹腔注射生理盐水(同对照组),皮下免疫猪TG 0.1 mg,在喂养第4、8周时分别再加强免疫1次,剂量减半;HI+Poly组:给药方法同HI组和Poly组;HI+TG组:给药方法同HI组和TG组.喂养8周后处死小鼠,取出甲状腺组织,冰冻切片、常规HE染色,光镜下观察小鼠甲状腺组织形态学变化:根据甲状腺组织炎细胞浸润数量及浸润范围、滤泡破坏范围等进行炎症程度分级;应用TLR3抗体对甲状腺切片进行免疫荧光染色,荧光显微镜下观察TLR3的表达,体视学分析甲状腺TLR3阳性细胞数密度变化.结果光镜下,Poly组甲状腺未见炎细胞浸润,HI组和TG组小鼠甲状腺都有不同程度的炎细胞浸润,HI+TG组和HI+Poly组甲状腺炎症细胞浸润和甲状腺滤泡破坏严重,炎症分级均在"++"以上.免疫荧光显示.HI组和Poly组的甲状腺滤泡上皮细胞可见到TLR3表达,在HI组和HI+Poly组炎症区域出现TLR3表达强阳性的炎症细胞.体视学分析甲状腺TLR3阳性细胞数密度,对照组、HI组、Poly组、TG组、HI+TG组、HI+Poly组组间比较差异有统计学意义(F=7.870,P<0.01);与对照组[(0.062±0.025)mm2]比较,HI+Poly组[(9.287±0.522)mm2]增加最为显著(P<0.01),而且HI+Poly组高于HI组[(2.570±0.257)mm2]和Poly组[(1.361±0.148)mm2,P均<0.01],HI+TG组[(4.843±0.405)mm2]高于HI组和TG组[(1.601±0.268)mm2,P均<0.01].结论 HI和TG免疫可诱发NOD鼠发生甲状腺炎,并刺激甲状腺滤泡上皮表达TLR3,Poly加重了HI诱发的NOD鼠甲状腺炎的病理变化过程;浸润的炎症细胞中亦有TLR3强阳性的细胞,提示TLR3途径参与了自身免疫性甲状腺炎的发病过程.     

扩张型心肌病的相关危险因素研究

目的 探讨扩张型心肌病(DCM)与环境化学元素、病毒感染及其他相关因素的关系.方法 2008年,在山东省阳谷县人民医院选择233例DCM患者(病例组)与150例稳定型心绞痛患者(对照组),对2组患者进行一般情况、疾病史调查,应用酶联免疫吸附试验(ELISA)测定病例组和对照组血清中人心肌抗体-IgG、柯萨奇B组病毒-IgG及腺病毒-IgG,应用原子吸收光谱法测定血清铜、锌、钙、镁、铁、锰等微量元素水平.并测定DCM高发区(阳谷县)和低发区(高唐县和临清市)饮用水一般化学指标及毒理指标.结果 ①病例组农民的比例[77.68%(181/233)]高于对照组[60.00%(90/150),χ2=13.8,P<0.01)],病例组人均年收入[(3207.82±618.51)元]低于对照组[(5086.61±886.12)元,t=24.40,P<0.01],病例组人均饮酒量[(175.02±160.50)g/d]高于对照组[(110.22±100.03)g/d,t=4.40,P<0.01],病例组心肌炎病史比例[5.15%(12/233)]高于对照组[0.67%(1/150),χ2=5.60,P<0.01].②DCM病人心肌抗体-IgG、人柯萨奇B组病毒-IgG及人腺病毒-IgG的阳性率分别为7.78%(7/90)、6.67%(6/90)及6.67%(6/90),对照组阳性率分别为3.33%(2/60)、5.00%(3/60)及5.00%(3/60),二者比较差异均无统计学意义(χ2值分别为1.26、0.18、0.18;P均>0.05).③DCM高发区饮用水含铁量、含锰量[(1.36±2.18)mg/L、(0.38±0.35)mg/L]高于低发区[(0.39±0.67)mg/L,(0.15±0.14)mg/L,t值分别为2.11、3.01,P均<0.01].④病例组血清含铁量[(69.1±57.8)μmol/L]高于正常值(15.6～35.9 μmol/L),且高于对照组[(20.0±17.5)μmol/L,t=5.04,P<0.01].结论 不支持DCM的发生与持续性病毒感染和自身免疫反应有关;DCM的发病可能与经济收入、饮酒量、心肌炎、饮用水中铁和锰及血清铁水平超标有一定关系.     

碘/钠摄入量对小鼠血脂代谢影响的实验研究

目的 探讨膳食碘摄入量对适钠和低钠饮食小鼠血脂代谢影响,为揭示碘与心血管疾病发病的相关性进行初步研究.方法 Balb/c小鼠260只,按体质量、性别随机分为适钠组(Na)和低钠组(Lna),每组130只;此两大组又分别按照碘摄入量分为①重度低碘组(SID);②轻度低碘组(MID);③适碘组(NI);④10倍碘过量组(10HI);⑤50倍碘过量组(50HI),总计为10组,每组26只.各组小鼠在饲养8个月时收集尿液和小鼠外周血,分离血清.测定小鼠尿碘、体质量、血脂[甘油三酯(TG)、总胆固醇(TC)、低密度脂蛋白(LDL)、高密度脂蛋白醇(HDL)]及甲状腺激素水平[总甲状腺素(TT4),总三碘甲腺原氨酸(TT3)、游离甲状腺素(FT4)、游离三碘甲腺原氨酸(FT3)].结果适钠组中,SID组、MID组雄性小鼠TG水平[(1.64±0.35)、(1.67±0.31)mmol/L]和SID组TC水平[(3.88±0.35)mmol/L]明显高于NI组[(1.49±0.42)、(3.25±0.47)mmol/L,P均＜0.05],SID组中雌性小鼠TG水平[(1.52±0.22)mmol/L]高于NI组[(1.23±0.22)mmol/L,P＜0.05].10HI和50HI组雄性小鼠外周血TG水平[(1.16±0.23)、(1.21±0.27)mmol/L]低于NI组(P均＜0.05),雌性小鼠TC水平[(2.37±0.49)、(2.48±0.37)mmol/L)低于NI组[(2.84±0.37)mmol/L,P均＜0.05].在低钠组,SID组雄性小鼠TG、TC水平[(1.39±0.40)、(3.33±0.46)mmol/L]均高于NI组[(1.30±0.28)、(3.00±0.53)mmol/L,P均＜0.05],SID组雌性小鼠TG、TC、LDL水平[(1.48±0.26)、(276±0.43)、(0.62±0.22)mmol/L]、MID组雌性小鼠LDL水平[(0.60±0.17)mmol/L]均高于NI组[(1.22±0.36)、(2.51±0.38)、(0.48±0.08)mmol/L,P均＜0.05].10HI和50HI组雄性小鼠TG水平[(1.12±0.22)、(0.90±0.11)mmol/L]均低于NI组(P均＜0.05),10HI和50HI组雌性小鼠TC水平[(2.35±0.34)、(2.37±0.37)mmol/L]、50HI组雌性小鼠LDL水平[(0.65±0.18)mmol/L]均低于NI组(P均＜0.05).适钠组中的SID和MID组血清TT4[(0.00±0.00)、(17.15±15.26)nmol/L]、FT4[(0.93±0.42)、(18.46±4.31)pmol/L]和TT3[(0.49±0.07)、(0.67±0.10)nmol/L]、FT3[(2.86±0.37)、(3.18±0.24)pmol/L]水平均低于NI组[(37.15±15.26)、(28.46±4.31)、(0.85±0.10)、(3.87±0.24)pmol/L,P＜0.01或P＜0.05].在低钠组,SID和MID组血清TT4、FT4和TT3、FT3水平[(0.00±0.00)nmol/L、(1.03±0.78)pmol/L、(0.51±0.05)nmol/L,(3.01±0.17)pmol/L,(19.76±12.22)nmol/L、(21.46±5.37)pmol/L、(0.71±0.21)nmol/L、(3.56±0.23)pmol/L]均低于NI组[(36.23±14.72)nmol/L、(30.96±6.33)pmol/L、(0.89±0.20)nmol/L、(4.05±0.24)pmol/L,P均＜0.05],10HI组的TT3水平[(1.06±0.23)nmol/L]高于NI组(P＜0.05).结论碘缺乏可致TG、TC和LDL升高,过量碘可致TG/TC水平降低.碘摄入量是影响血脂代谢的重要因素.限盐饮食的同时,严密监控碘的摄入量对当前有效防治心血管疾病应具有重要作用.     

过氧化物酶体增殖物激活受体-γ对干燥综合征非肥胖型糖尿病小鼠的抗炎作用

目的 探讨过氧化物酶体增殖物激活受体(PPAR)-γ对干燥综合征(SS)动物模型非肥胖型糖尿病(NOD)小鼠的抗炎作用.方法 8周龄NOD小鼠20只,随机分为2组,每组10只.实验组自9周龄给予罗格列酮按40 mg/kg剂量隔天灌胃.分别在12周龄和15周龄时随机处死罗格列酮组和对照组各1只小鼠,17周龄时处死全部小鼠,留取外周血和唇腺组织.用苏木素-伊红(HE)染色评价唇腺的病理学改变.酶联免疫吸附试验(ELISA)法测定外周血中白细胞介素(IL)-1β、IL-4、IL-6和肿瘤坏死因子(TNF)-α的含量.实时荧光定量反转录-聚合酶链反应(real-time PCR)检测唇腺组织中IL-1β、IL-4、IL-6和TNF-α mRNA的表达量.计量资料两样本间比较采用t检验.结果 罗格列酮组小鼠唇腺组织中单核细胞浸润较对照组均减轻,腺体破坏少.17周龄时罗格列酮组与对照组比较,外周血IL-6[(26±7)与(37±11),t=-2.298]和TNF-α[(57±22)与(79±21),t=-2.188]的含量明显减少(P<0.05);IL-4[(26±13)与(12±4),t=2.438]的含量明显增加(P<0.05);唇腺组织中TNF-α mRNA的表达水平明显降低;而IL-4 mRNA的表达水平明显升高(P<0.05).结论 PPAR-γ对NOD小鼠干燥综合征有疗效,其作用机制可能与其下调SS体内Th1细胞因子、使Th1/Th2平衡向Th2方向转化相关.

Abstract：

Objective To investigate the anti-inflammatory effect of peroxisome proliferator-activated receptor-γ(PPAR-γ)in non-obese diabetic mice(NOD mice)with Sj(o)gren's syndrome(SS)．Methods Twenty 8-weeks-old female NOD mice were randomly divided into 2 groups．Rosiglitazone and normal saline were administered for the rosiglitazone group and control group respectively．At age of 12 weeks and 15 weeks,one mouse in the rosiglitazone group and the control group were killed respectively,and the others were sacrificed at the age of 17 weeks．Blood were obtained by cardiac puncture,and minor salivary glands (MSG) were resected．The histopathological changes waere examined by H&E staining．The level of IL-1β,IL-4,IL-6 and TNF-α in serum were measured by ELISA．Real-time PCR waft used to evaluate the mRNA expression level of IL-1β,IL-4,IL-6 and TNF-α in MSG．Student's t-test was used to assess the differences．Results Compared with the control group,the mice in the rosiglitazone group showed that：①histopatho-logical change was significantly ameliorated．②At the age of 17 weeks,IL-6[(26±7)vs(37±11),t=-2．298] and TNF-α[(57±22)vs(79±21),t=-2．188] were expressed significantly lower and IL-4[(26±13)vs(12±4),t=2．438 ] was expressed significantly higher in serum(P<0．05)．③The expression of TNF-αwas significantly decreased and the expression of IL-4 was significantly increased in MSG (P<0．05)．Conclusion PPAR-γ can ameliorate SS on NOD mice effectively．The mechanism may be related to reduction of Th1 cytokines,and the Th1/Th2 balance is changed into Th2 predominant．     

胰岛素样生长因子Ⅰ在碘缺乏和碘过量小鼠甲状腺形态变化中的作用

目的 观察碘缺乏和碘过量小鼠甲状腺胰岛素样生长因子Ⅰ(IGF-Ⅰ)的水平及在甲状腺形态变化中的作用.方法 选用Balb/c小鼠48只,体质量约16 g,雌雄各半.按体质量、性别将小鼠随机分为3组:碘缺乏组(LI,饲料中含碘量为50μg/kg,饮去离子水);适碘组(对照,NI,饲料中含碘量为300μg/kg,饮去离子水)、碘过量组(HI,饲料中含碘量为300μg/kg,饮水中含碘量14 700μg/kg);每组16只.喂养12周后处死,取小鼠甲状腺,测量甲状腺的绝对及相对质量,HE染色,光镜下观察小鼠甲状腺的形态学变化;RT-PCR法检测IGF-Ⅰ mRNA表达:免疫组化法检测甲状腺IGF-Ⅰ蛋白质表达.结果 小鼠甲状腺的绝对质量和相对质量,组间比较差异有统计学意义(F值分别为315.881、405.921,P均<0.01);其中LI组[(10.71±4.03)mg,(44.98±15.39)mg/100 g体质量]和HI组[(3.42±1.17)mg,(13.50±3.89)mg/100 g体质量]高于NI组[(2.11±0.53)mg,(8.35±1.98)mg/100 g体质量,P均<0.01].光镜下,LI组小鼠滤泡体积变小,数量增多,上皮细胞呈柱状或高柱状,增生呈复层,滤泡腔内胶质减少或缺如;而HI组小鼠发生了胶质蓄积,滤泡增大,未见滤泡增生.甲状腺IGF-Ⅰ mRNA表达,LI组(1.03±0.32)明显高于NI组(0.65±0.19),组间比较差异有统计学意义(F=7.518,P<0.01),HI组与NI组比较有下降趋势,但差异无统计学意义(P>0.05).甲状腺IGF-Ⅰ蛋白质表达,LI组小鼠甲状腺滤泡上皮细胞内棕黄色颗粒明显多于NI组和HI组,而HI组却少于NI组.结论 碘缺乏和碘过量小鼠发生甲状腺肿,甲状腺IGF-Ⅰ mRNA和蛋白表达的改变,可能参与碘缺乏和碘过量导致甲状腺形态改变的过程,甲状腺白分泌的IGF-Ⅰ在缺碘性和高碘性甲状腺肿形成过程中可能起重要调节作用.     

冠状动脉血流缓慢患者临床及造影结果的特点分析

目的 探讨冠状动脉血流缓慢(SCF)的临床特点及实验室检查的相关性.方法 通过TIMI血流分级法和TIMI帧数法联合判断,入选2008年1月至2009年12月因胸痛等心肌缺血症状于复旦大学附属中山医院心内科行冠状动脉造影(CAG)示心外膜冠状动脉无明显病变但存在SCF的患者共140例,对照组为连续性入选同期行CAG证实心外膜冠状动脉完全正常且血流正常的患者共140例.入院时记录所有研究对象的临床资料,测量并记录糖代谢、脂代谢等实验室指标,并进行统计学分析.结果 (1)SCF组的年龄小于对照组[(57.8±10.7)岁比(59.8±8.2)岁,P<0.01],糖尿病病史(49.3% 比 30.7%)、目前吸烟率(59.3%比46.4%)均高于对照组(P均<0.05),空腹血糖(FBG)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)/高密度脂蛋白胆固醇(HDL-C)(2.76±1.19比2.37±1.14)、载脂蛋白B(apoB)/载脂蛋白A1(apoA1)(0.95±0.27比0.83±0.55)水平高于对照组(P均<0.05),HDL-C[(1.05±0.35)mmol/L比(1.42±0.74)mmol/L]和apoA1[(1.10±0.19)mmol/L比(1.31±0.31)mmol/L]水平低于对照组(P均<0.01).(2)140例SCF患者中,最常见的血管受累情况是三支血管同时存在SCF(92例),而最常见的受累血管为右冠状动脉(RCA)(119例).(3)多因素logistic回归分析显示在调整其他因素的影响后,吸烟(OR=1.92,95% CI:1.04～3.57,P<0.05)、糖尿病(OR=2.44,95% CI:1.32～4.76,P<0.01)、FBG异常(OR=2.13,95% CI:1.16～3.98,P<0.05)、TG(OR=1.47,95% CI:1.03～2.13,P<0.05)、HDL-C(OR=0.47,95% CI:0.24～0.85,P<0.05)及apoA1(OR=0.55,95% CI:0.40～0.75,P<0.01)是发生SCF的独立预测因子.结论 年轻的吸烟患者更容易发生SCF,SCF患者存在糖代谢和脂代谢异常,脂代谢异常表现为TG升高、HDL-C水平下降.

Abstract：

Objective To analyze the clinical and angiographic characteristics of patients with slow coronary flow (SCF). Methods In this retrospective study, 140 patients with SCF and 140 control subjects without SCF were included. SCF were diagnosed by the combination of TIMI flow grade method and TIMI frame count method. All subjects had angiographically normal coronary arteries. The clinical and laboratory data were obtained from medical records at admission. Results Compared to control group, patients with SCF were younger [(57.8±10.7)years vs. (59.8±8.2)years], rate of smokers (59.3% vs. 46.4%) and diabetes mellitus (49.3% vs. 30.7%), fasting blood glucose (FBG) level [(7.8±2.8) mmol/L vs. (6.2±2.0) mmol/L, P<0.05] and triglyceride (TG) level [(2.11±1.93) mmol/L vs. (1.67±1.01) mmol/L,P<0.05] were higher, while high density lipoprotein cholesterol (HDL-C) level [(1.05±0.35) mmol/L vs. (1.42±0.74) mmol/L, P<0.01] and apolipoprotein A1(apoA1) level [(1.10±0.19)mmol/L vs. (1.31±0.31)mmol/L, P<0.01] were lower. Among the 140 SCF patients, left anterior descending artery (LAD), left circumflex artery (LCX) and right coronary artery (RCA) were involved at the same time in 92 patients. Among the three vessels, RCA is the most frequent involved vessel (n=119). After adjusting for other risk factors, current smoking (OR=1.92,95% CI:1.04-3.57,P<0.05), DM history (OR=2.44,95% CI:1.32-4.76,P<0.01), FBG (OR=2.13,95% CI:1.16-3.98,P<0.05), TG (OR=1.47,95% CI:1.03-2.13,P<0.05), HDL-C (OR=0.47,95% CI:0.24-0.85,P<0.05) and apoA1 (OR=0.55,95% CI:0.40-0.75,P<0.01) were independent factors for SCF (all P<0.05). Conclusions Our results demonstrated that patients with SCF were prone to have a significant metabolic disorder compared to the control group. Patients with high levels of FBG, TG and low levels of HDL-C were more likely to suffer from SCF, which maybe explained by the development of coronary endothelium and microvascular dysfunction.