The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

The expression of NF-κB and TGF-β1 in the injured kidneys of neonate rats with endotoxemia

Objective To investigate the mechanism of the kidney injure in the newborn rats with endotoxemia.Methods Eighty Wistar rats aged 7 days were randomly divided into 2 groups:control group (intraperitoneal injection of saline of 0.1 ml;n = 40),lipopolysaccharide(LPS) group(intraperitoneal injection of LPS of 5 mg/kg;n =40).The rats in either group were killed at 1 h,4 h,8 h and 12 hours after intraperitoneal injection,respectively.The expressions of NF-κB and TGF-β1 in the kidney were detected by using the immunohistochemical assay.Renal ultrastructural changes was observed with a CM100 Philips electron microscope.Results The NF-κB in control group had no expression.NF-κB in LPS group mainly expressed in the renal tubular epithelial cell,increased at 1 h after test and peaked at 8 h,and slightly descended at 12 h.The expression of TGF-β1 in control group was slight,and had not show significant difference from control group at 1 h,4 h and 8 h,but significantly higher than that in control group at 12 h.In LPS group,newborn rat renal glomerular basement membrane was complete,part epithelial cell foot processes were fused and renal tubules epithelial cell mild mitochondria vacuolization was found at 4 h.Renal glomeruli epithelial cell foot processes obvious confluenced,quantities of mesangial cells mitochondria vacuole,and renal tubules epithelial cell mitochondria expanded to bubbles at 12 h.Conclusion The NF-κB involves in the pathogenesis of kidney damage induced by endotoxemia,but TGF-β1 may help to repair the damaged kidney,and may repress the production of NF-κB.     

内毒素诱导幼年大鼠脑神经细胞凋亡及脑组织ERK表达的变化

Objective To investigate the effect of ERK in apoptosis of neuron induced by endotoxemia,provide the theory basis for the early intervention. Methods Wistar rats aged 10 day were randomly divided into two groups:LPS group and NS group. Neuron apoptosis at 6、12、72 h after abdomen injection were detected by TUNEL method, the expressions of ERK were measured by immunohistochemial method.Results ( 1 ) apoptosis cell appeared at 6 hour in LPS group, but the apoptosis index showed no difference from NS group( P ＞ 0. 05 ). The apoptosis cell obvious increased at 12 hour, peaked at 72 hour( P ＜ 0. 05 ,P ＜0. 01 ). (2) As compared with NS group, the expression of ERK increased at 6 h ( P ＜ 0. 01 ), obviously decreased at 12 h(P ＜0. 01 ) ,and reversed to the level of NS group at 72 h(P ＞0. 05). Conclusion LPS can induce the neuron apoptosis in young rats, the ERK is activated and could play role in apoptosis.     

Effect of epigallocatechin-3-gallate (EGCG) on the expressions of nuclear faclor-E2 related factor2 (Nrf2)and γ-glutamylcystein synthase (γ-GCS) in renal tubular epithelial cells of rats with oxidative Stress

Objective To investigate the mechanism of antioxygen reaction of epigallocatechin-3-gallate (EGCG) in renal tubular epithelial cells of rats with oxidative stress induced by H2O2. Methods Cultured cells were divided into control group, H2O2 group and EGCG group. Cell survival was observed with MTT. The expressions of Nrf2 mRNA and -γ-GCS mRNA in cultured cells were examined by real time quantitative PCR. Immunohistochemistry and western blotting were used to detecte the expressions of Nrf2 and γ-GCS protein. Results The survival rate of tubular cells was 97. 61 ± 6.33 in control group. There was a significant decrease in H2 O2 group (56. 38 ± 5.57) (P < 0.01), while increased when the EGCG concentration were 5,10,20 mg/L(77.42 ±5.31,83.27 ±5.94,90.24 ±5.72) (P <0.05,P <0.01). EGCG up-regulated the expressions of Nrf2 and γ-GCS mRNA and protein in renal tubular epithelial cells with dose depen-dentment. Conclusion The expressions of Nrf2 and-γ-GCS increase in renal tubular epithelial cells with oxidative stress. Resulting from suppression of oxidative stress,EGCG exerts protective effect on NRK,and this antioxidative effect may be partly induced by activating the Nrf2 signal pathway.     

Effect of epigallocatechin-3-gallate (EGCG) on the expressions of nuclear faclor-E2 related factor2 (Nrf2)and γ-glutamylcystein synthase (γ-GCS) in renal tubular epithelial cells of rats with oxidative Stress

Objective To investigate the mechanism of antioxygen reaction of epigallocatechin-3-gallate (EGCG) in renal tubular epithelial cells of rats with oxidative stress induced by H2O2. Methods Cultured cells were divided into control group, H2O2 group and EGCG group. Cell survival was observed with MTT. The expressions of Nrf2 mRNA and -γ-GCS mRNA in cultured cells were examined by real time quantitative PCR. Immunohistochemistry and western blotting were used to detecte the expressions of Nrf2 and γ-GCS protein. Results The survival rate of tubular cells was 97. 61 ± 6.33 in control group. There was a significant decrease in H2 O2 group (56. 38 ± 5.57) (P < 0.01), while increased when the EGCG concentration were 5,10,20 mg/L(77.42 ±5.31,83.27 ±5.94,90.24 ±5.72) (P <0.05,P <0.01). EGCG up-regulated the expressions of Nrf2 and γ-GCS mRNA and protein in renal tubular epithelial cells with dose depen-dentment. Conclusion The expressions of Nrf2 and-γ-GCS increase in renal tubular epithelial cells with oxidative stress. Resulting from suppression of oxidative stress,EGCG exerts protective effect on NRK,and this antioxidative effect may be partly induced by activating the Nrf2 signal pathway.     

单侧隐睾大鼠对侧睾丸组织中SCF/c-kit基因表达变化及意义

Objective To investigate the pathologic changes and expressions of SCF and c-kit in the contralateral testes in rat model of unilateral cryptorchidism. Methods Thirty male SD rats were maintained under controlled temperature and constant photoperiodic conditions with access to food and water. The rats were randomly assaigned to the control group and the experimental unilateral cryptorchidism group. The left testis of the rats in the unilateral cryptorchidism group was placed into the abdominal cavity. The control group rats were subjected to sham surgery. Three months later, the rats were sacrificed and their right testes were harvested. The pathological changes were observed under microscope. The mRNA and protein expression of SCF and c-kit were also investigated using quantitative Real-time RT-PCR, Western blotting and immunohistochemical staining. Apoptotic germ cells were detected by TUNEL staining. Results All rats survived to the endpoints. The right testes of rats of the unilateral cryptorichid group were smaller than those of the control group. Normal testes of the control group rats manifested active spermatogenesis and orderly arrangement of germ cells.However, disordered and sloughed germinal cells with less distinct seminiferous tubule borders were observed in the contralateral testes of rats with experimental unilateral cryptorichid under the microscope. Cmpared with the control testes, the mRNA and protein expression of SCF and c-kit of the contralateral testes of rats with experimental unilateral cryptorichid was decreased (P＜0.05). The apoptotic germ cells were increased (19.7±3.83 vs 5. 4 ± 1.02, P＜0. 05). The SCF/c-kit expression was positively correlated with the germ cell apoptosis (P＜0. 01 ). Conclusions The decreased expression of SCF and c-kit and increased germ cell apoptosis are found in the contralateral testes, which may contribute to thc infertility in the rat model of experimental unilateral cryptorchidism.     

高氧致慢性肺疾病新生大鼠肺泡损伤及肺泡上皮细胞的变化

Objective To explore the changes of alveolar morphology and alveolar epithelial cells in rats with hyperoxia-induced chronic lung diseases (CLD). Methods CLD model in neonatal rats was established by inhalation of high concentration oxygen(85%～90% ). Eighty neonatal rats were randomly exposed to hyperoxia (model group) and to room air (control group) (n =40 each). Radical alveolar counts and the alveolar septum thickness were used to evaluate alveolar development. The site and intensity of expression of SPC,AQP5 protein were detected by immunohistochemical staining,the dynamic expression of SPC mRNA,AQP5mRNA was detected by RT-PCR on day 1,3,7,14 and 21 after exposure. Results There were no significant differences about alveolar wall thickness and RAC between experimental groups and control group on day 1～3 ( P > 0. 05 ). But there was significant difference between the model group and the control groups on day 7 and 14 (P <0. 01 ). For model group,alveolar septum thickness peaked on day 21, the difference was significant compared with control group ( 10. 62±5.01 vs 3.62±0. 88, P < 0. 001 ), but RAC decreased to the lowest level, the difference was significant compared with control group ( 3.57±1.24 vs 10. 47±0. 88,P <0. 001 ). The expression of SPC decreased on day 3 manifestedly but increased on day 7 and the levels of SPC were higher than that in the control group. Experimental group showed gradual decrease in AQP5 expression as the lung impairment devastated. Conclusion Alveolar development was delayed and alveolar epithelial cell (AEC) was damaged in the neonatal CLD rats. The changes of SPC,AQP5 expression suggested AECI was severely damaged and failed in full recovery, meanwhile the quantity of AEC Ⅱ was increased but the ability of its differentiation and transformation was decreased.     

高氧致慢性肺疾病新生大鼠肺泡损伤及肺泡上皮细胞的变化

Objective To explore the changes of alveolar morphology and alveolar epithelial cells in rats with hyperoxia-induced chronic lung diseases (CLD). Methods CLD model in neonatal rats was established by inhalation of high concentration oxygen(85%～90% ). Eighty neonatal rats were randomly exposed to hyperoxia (model group) and to room air (control group) (n =40 each). Radical alveolar counts and the alveolar septum thickness were used to evaluate alveolar development. The site and intensity of expression of SPC,AQP5 protein were detected by immunohistochemical staining,the dynamic expression of SPC mRNA,AQP5mRNA was detected by RT-PCR on day 1,3,7,14 and 21 after exposure. Results There were no significant differences about alveolar wall thickness and RAC between experimental groups and control group on day 1～3 ( P > 0. 05 ). But there was significant difference between the model group and the control groups on day 7 and 14 (P <0. 01 ). For model group,alveolar septum thickness peaked on day 21, the difference was significant compared with control group ( 10. 62±5.01 vs 3.62±0. 88, P < 0. 001 ), but RAC decreased to the lowest level, the difference was significant compared with control group ( 3.57±1.24 vs 10. 47±0. 88,P <0. 001 ). The expression of SPC decreased on day 3 manifestedly but increased on day 7 and the levels of SPC were higher than that in the control group. Experimental group showed gradual decrease in AQP5 expression as the lung impairment devastated. Conclusion Alveolar development was delayed and alveolar epithelial cell (AEC) was damaged in the neonatal CLD rats. The changes of SPC,AQP5 expression suggested AECI was severely damaged and failed in full recovery, meanwhile the quantity of AEC Ⅱ was increased but the ability of its differentiation and transformation was decreased.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.     

缺氧缺血性脑损伤新生大鼠脑组织MMP-9和TIMP-1表达的动态变化研究

Objective To explore the mechanism of hypoxic-ischemic brain damage(HIBD) and provide new ideas for clinical treatment of hypoxic-iscbemic encephalopathy.Methods Neonatal 7-day-old Wistar rats were randomly divided into sham-operation control group,HIBD 6 h,12 h,24 h,48 h and 72 h groups(n =6 per group).The model of HIBD was induced by unilateral carotid ligation followed by timed exposure to 8% oxygen.The expression of MMP-9 mRNA and TIMP-1 mRNA in brain tissue of neonatal rats was measured by Real-time Q-PCR method.Results (1) The ligatod brainhemisphere of HIBD groups showed obvious edema from 12 h to 48 h after hypoxia -ischemia in the neonatal rats.(2) The expression of MMP-9 mRNA was very low in the sham-operation control group,but in HIBD groups,it began to increase at 6 h,and reached a peak at 24 h,then gradually decreased,but still maintained at high level at 72 h(P＜0.01).(3) The expression of TIMP-1 mRNA was aslo very low in the sham-operation control group.But in HIBD group,it increased slightly at 6 h,12 h and 24 h,compared to the sham-operation control group,each group was statistically significant(P＜0.05),with no significant difference among the three groups(P＞0.05),then decreased at 48 h and 72 h,but with no significant difference from sham-operation control group (P＞ 0.05).(4) The ratio of MMP-9 mRNA/TIMP-1 mRNA was normal in the sham-operation control group and HIBD 6 h group,it began to increase at 12 h,and reached a peak at 48 h,then gradually decreased,but still maintained at high level at 72 h(P ＜0.01).Conclusion Hypoxia-ischemia increases the expression of MMP-9 mRNA in brain tissue of nenatal rats,and the imbalance in the expression of MMP-9 mRNA and TIMP-1 mRNA possibly is one cause of brain edema induced by HIBD.