Protective effect of intense pulsed light on fibroblast injury induced by UVA Ⅰ

Objective To study the protective effects of intense pulse light (IPL) on the injury of normal human skin fibroblasts (FB) induced by ultraviolet A (UVA Ⅰ ) in vitro and to explore its possible mechanism. Methods The human skin fibroblasts were isolated and cultured, and then irradiated by UVA Ⅰ (9 J/cm2) and IPL (15 J/cm2), respectively. The proliferative ability of the cells were detected by CCK-8. Cell cycle was detected by flow cytometry, and cylin D1 and CDK2 protein expression levels were detected by Western blot. Results Different doses of UVA Ⅰ irradiation caused certain damages of cultured fibroblasts. With the increasing of of UVA Ⅰ dose, cell proliferation was decreased. Cells went to death at the exposure to 11 J/cm2 UVA Ⅰ , while the proliferative activity did not change much at 7 J/cm2 UVA Ⅰ . Cells were treated with UVA Ⅰ for other 2 days, then with IPL irradiation for other 2days, showing clear stimulating to the cell proliferation as compared with the cells that received UVA Ⅰ treatment only. Flow cytometry results showed that an increase of cell proliferating index, and cell cycle protein cyclin D1 and CDK2 expression levels were also upregulated after IPL irradiation.Conclusion UVA Ⅰ irradiation may cause cell damage as showed by cell growth index, cyclin D1 and CDK2 expression, and this injury could be protected partly by IPL treatment. The intense pulsed light may regulate the expression of cyclin proteins that may promote normal fibroblast proliferation, which could be one of the mechanisms of IPL skin rejuvenation.     

组织蛋白酶G在光老化皮肤成纤维细胞中的表达及意义

Objective To investigate the role of cathepsin G in photoaged fibroblasts. Methods Human fibroblasts were cultured and induced to premature senescence using UVA + MOP methods. Senescence-associated-β-galactosidase (SA-β-gal) stain was used to evaluate the positive rate of aged cells. The mRNA and protein expression of cathepsin G in photoaged fibroblasts were detected by real-time RT-PCR and Western blot techniques. Results Over 98 % induced cells presented a positive SA-β-gal straining. The expression of cathepsin G, detected by Western blot, was increased to (1. 70±0. 028) times of the control. And RT-PCR revealed that the synthesis of cathepsin G mRNA was also up-regulated to 1. 42±0. 09. Conclusion The results of our study demonstrates a significant correlation between photoaged fibroblasts and cathepsin G. The up-regulation of cathepsin G may play an important role in the damages of extracellular matrix and activation of MMPS in photoaged human skin.     

组织蛋白酶G在光老化皮肤成纤维细胞中的表达及意义

Objective To investigate the role of cathepsin G in photoaged fibroblasts. Methods Human fibroblasts were cultured and induced to premature senescence using UVA + MOP methods. Senescence-associated-β-galactosidase (SA-β-gal) stain was used to evaluate the positive rate of aged cells. The mRNA and protein expression of cathepsin G in photoaged fibroblasts were detected by real-time RT-PCR and Western blot techniques. Results Over 98 % induced cells presented a positive SA-β-gal straining. The expression of cathepsin G, detected by Western blot, was increased to (1. 70±0. 028) times of the control. And RT-PCR revealed that the synthesis of cathepsin G mRNA was also up-regulated to 1. 42±0. 09. Conclusion The results of our study demonstrates a significant correlation between photoaged fibroblasts and cathepsin G. The up-regulation of cathepsin G may play an important role in the damages of extracellular matrix and activation of MMPS in photoaged human skin.     

AA-861抑制5-LO途径对KC和HSC的影响

Objective To investigate the effects of AA-861, the specific inhibitor of 5-lipoxyge-nase (5-LO), on the activation, proliferation and gene expression of kupffer cell (KC) and hepatic stellate cell (HSC). Methods 1) After being exposed to AA-861, the gene expression, proliferative ability and apoptosis of activated KC induced by lipopolysaecharide (LPS) were detected; 2) After the activated KC being exposed to AA-861, the supernatant of KC was added into quiescent HSC, then the proliferative ability and gene expression of quiescent HSC were observed. Results 1) After being activated by LPS, the mRNA and protein expression of 5-LO in KC increased remarkably while the mRNA and protein expression of 5-LO and 5-LO production decreased significantly after KC being ex-posed to AA-861. 2) After the supernatant of activated KC was added into quiescent HSC, the prolif-erative ability and gene expression of Collagen-1, α-SMA and TIMP-1 were increased significantly. However, after the supernatant of activated KC being exposed to AA-861 was added to quiescent HSC, it inhibited the activation of quiescent HSC and the proliferative ability and gene expression of HSC were decreased. Conclusion Inhibition of the 5-LO pathway by AA-861 can induce the over-pro-liferated KC to undergo apoptosis, and then inhibit the activation and proliferation of HSC and de-crease the production of ECM.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Effects of α1-adrenergic receptor on the proliferation of cholangiocarcinoma cells

Objective To investigate the correlation between α1-adrenergic receptor and the pathological behavior of cholangiocarcinoma, and the effects of norepinephrine (NE) on the proliferation of cholangiocarcinoma cell line QBC939. Methods Thirty-six samples of cholangiocarcinoma were resected in Southwest Hospital from August 2002 to March 2008. The expression of α1-adrenergic receptor in the 36 samples of cholangiocarcinoma tissue and 4 samples of normal bile duct tissue were detected by SABC technique. The proliferation of cholangio-carcinoma cell line QBC939 was detected after processing the cells with NE, phentolamine and prazosin. All the data were analyzed by chi-square test. Results The high positive expression rate of α1-adrenergic receptor was 68% (17/25) in patients with lymph node metastasis, which was significantly higher than 9% (1/11) in patients without lymph node metastasis (χ2=10.604, P<0.05). The high positive expression rate of α1-adrenergic receptor was 85% (11/13) in patients with middle and low positioned cholangiocarcinoma, which was significantly higher than 30% (7/23) in patients with hilar cholangiocarcinoma (χ2=9.753, P<0.05). NE promoted the proliferation of cholangiocarcinoma cell line QBC939 by stimulating the expression of α1-adrenergic receptor, and in a concentration-dependent manner. The proliferative effect was weakened as time passed by, and it was eliminated by phentolamine and prazosin. Conclusions The expression of α1-adrenergic receptor is diverse due to lymph node metastasis and the location of the tumor, α1-adrenergic receptor with high expression may play an important role in the proliferation and metastasis of cholangiocarcinoma.     

Nd:YAG激光与强脉冲光非剥脱性嫩肤的动物实验

Objective To observe the histological change of different waves in treating SD rats of the long-pulse 1064nm Nd:YAG laser and the 560～1200 nm intense pulse light,in order to provide the theory bases of non-ablative rejuvenation.Methods Two waves were used on experimental mice.The dermic thickness and the expression of collagen typesⅠand Ⅲwere detected by HE stain and immunohistochemical methods. Semiquantitative analysis was used to determine the mean of absorbance.Results Thedermal thicknesses and the mean of absorbance of collagen typesⅠandⅢin two different waves were higher than those in common control groups(P＜0.05).The effect of Nd:YAG laser groups were higher than IPL groups(P＜0.05).The expression of collagen typeⅠwas higher than that of collagen type Ⅲ(P＜0.001).Conclusion After Nd:YAG laser or IPL irradiation,the dermal thickness and collagen typesⅠandⅢof SD rats are increased.The effects of Nd:YAG laser are better than those of 560～1 200 nm IPL.The expression of collagen type Ⅲ is obviously more than that of collagen typeⅠin the early,whereas the expression of collagen typeⅠis obviously more than that of collagen type Ⅲin the later.It proves that the mechanism of dermal remodeling of non-ablative skin rejuvenation is mainly correlation with raising range and time of collagen typeⅠ.     

结缔组织生长因子影响体外培养瘢痕成纤维细胞ERK/MAPK信号通路活化及增殖的研究

Objective To explore the signal mechanism of proliferation stimulating effect of connec-tive tissue growth factor (CTGF) on hypertrophic scar (HS) derived fibroblasts. Methods <'3>H-TdR in-corporation technique was used to determine the proliferative effect of CTGF at different concentration. Western blot was applied to semi-quantitively analyze the expression of phosphorylated and total ERK1/2 protein after 0, 5, 10, 15, 30, and 60 min of CTGF stimulation, and the relative value of which was de-fined as AI to measure the activation of ERK1/2 signal pathway. PD98059 was admitted to specifically block the ERK1/2 pathway, and subsequently cell proliferation stimulated by CTGF was studied by MTT. Results CTGF could stimulate fibroblasts proliferation with a dose-dependant manner, and activa-ted the ERK1/2 signal pathway, and AI built up to 0.209±0.0201, reaching the apex at 15 min after stimulation performed. Inhibition of ERK1/2 activation by PD98059 suppressed CTGF-mediated HS fi-broblasts proliferation significantly, while OD significantly dropped. Conclusion CTGF induces a prolif-erative response in HS fibroblasts, and this action is mainly dependent on the activation of ERK1/2 signal pathway.     

结缔组织生长因子影响体外培养瘢痕成纤维细胞ERK/MAPK信号通路活化及增殖的研究

Objective To explore the signal mechanism of proliferation stimulating effect of connec-tive tissue growth factor (CTGF) on hypertrophic scar (HS) derived fibroblasts. Methods <'3>H-TdR in-corporation technique was used to determine the proliferative effect of CTGF at different concentration. Western blot was applied to semi-quantitively analyze the expression of phosphorylated and total ERK1/2 protein after 0, 5, 10, 15, 30, and 60 min of CTGF stimulation, and the relative value of which was de-fined as AI to measure the activation of ERK1/2 signal pathway. PD98059 was admitted to specifically block the ERK1/2 pathway, and subsequently cell proliferation stimulated by CTGF was studied by MTT. Results CTGF could stimulate fibroblasts proliferation with a dose-dependant manner, and activa-ted the ERK1/2 signal pathway, and AI built up to 0.209±0.0201, reaching the apex at 15 min after stimulation performed. Inhibition of ERK1/2 activation by PD98059 suppressed CTGF-mediated HS fi-broblasts proliferation significantly, while OD significantly dropped. Conclusion CTGF induces a prolif-erative response in HS fibroblasts, and this action is mainly dependent on the activation of ERK1/2 signal pathway.     

结缔组织生长因子影响体外培养瘢痕成纤维细胞ERK/MAPK信号通路活化及增殖的研究

Objective To explore the signal mechanism of proliferation stimulating effect of connec-tive tissue growth factor (CTGF) on hypertrophic scar (HS) derived fibroblasts. Methods <'3>H-TdR in-corporation technique was used to determine the proliferative effect of CTGF at different concentration. Western blot was applied to semi-quantitively analyze the expression of phosphorylated and total ERK1/2 protein after 0, 5, 10, 15, 30, and 60 min of CTGF stimulation, and the relative value of which was de-fined as AI to measure the activation of ERK1/2 signal pathway. PD98059 was admitted to specifically block the ERK1/2 pathway, and subsequently cell proliferation stimulated by CTGF was studied by MTT. Results CTGF could stimulate fibroblasts proliferation with a dose-dependant manner, and activa-ted the ERK1/2 signal pathway, and AI built up to 0.209±0.0201, reaching the apex at 15 min after stimulation performed. Inhibition of ERK1/2 activation by PD98059 suppressed CTGF-mediated HS fi-broblasts proliferation significantly, while OD significantly dropped. Conclusion CTGF induces a prolif-erative response in HS fibroblasts, and this action is mainly dependent on the activation of ERK1/2 signal pathway.     

结缔组织生长因子影响体外培养瘢痕成纤维细胞ERK/MAPK信号通路活化及增殖的研究

Objective To explore the signal mechanism of proliferation stimulating effect of connec-tive tissue growth factor (CTGF) on hypertrophic scar (HS) derived fibroblasts. Methods <'3>H-TdR in-corporation technique was used to determine the proliferative effect of CTGF at different concentration. Western blot was applied to semi-quantitively analyze the expression of phosphorylated and total ERK1/2 protein after 0, 5, 10, 15, 30, and 60 min of CTGF stimulation, and the relative value of which was de-fined as AI to measure the activation of ERK1/2 signal pathway. PD98059 was admitted to specifically block the ERK1/2 pathway, and subsequently cell proliferation stimulated by CTGF was studied by MTT. Results CTGF could stimulate fibroblasts proliferation with a dose-dependant manner, and activa-ted the ERK1/2 signal pathway, and AI built up to 0.209±0.0201, reaching the apex at 15 min after stimulation performed. Inhibition of ERK1/2 activation by PD98059 suppressed CTGF-mediated HS fi-broblasts proliferation significantly, while OD significantly dropped. Conclusion CTGF induces a prolif-erative response in HS fibroblasts, and this action is mainly dependent on the activation of ERK1/2 signal pathway.     

结缔组织生长因子影响体外培养瘢痕成纤维细胞ERK/MAPK信号通路活化及增殖的研究

Objective To explore the signal mechanism of proliferation stimulating effect of connec-tive tissue growth factor (CTGF) on hypertrophic scar (HS) derived fibroblasts. Methods <'3>H-TdR in-corporation technique was used to determine the proliferative effect of CTGF at different concentration. Western blot was applied to semi-quantitively analyze the expression of phosphorylated and total ERK1/2 protein after 0, 5, 10, 15, 30, and 60 min of CTGF stimulation, and the relative value of which was de-fined as AI to measure the activation of ERK1/2 signal pathway. PD98059 was admitted to specifically block the ERK1/2 pathway, and subsequently cell proliferation stimulated by CTGF was studied by MTT. Results CTGF could stimulate fibroblasts proliferation with a dose-dependant manner, and activa-ted the ERK1/2 signal pathway, and AI built up to 0.209±0.0201, reaching the apex at 15 min after stimulation performed. Inhibition of ERK1/2 activation by PD98059 suppressed CTGF-mediated HS fi-broblasts proliferation significantly, while OD significantly dropped. Conclusion CTGF induces a prolif-erative response in HS fibroblasts, and this action is mainly dependent on the activation of ERK1/2 signal pathway.     

结缔组织生长因子影响体外培养瘢痕成纤维细胞ERK/MAPK信号通路活化及增殖的研究

Objective To explore the signal mechanism of proliferation stimulating effect of connec-tive tissue growth factor (CTGF) on hypertrophic scar (HS) derived fibroblasts. Methods <'3>H-TdR in-corporation technique was used to determine the proliferative effect of CTGF at different concentration. Western blot was applied to semi-quantitively analyze the expression of phosphorylated and total ERK1/2 protein after 0, 5, 10, 15, 30, and 60 min of CTGF stimulation, and the relative value of which was de-fined as AI to measure the activation of ERK1/2 signal pathway. PD98059 was admitted to specifically block the ERK1/2 pathway, and subsequently cell proliferation stimulated by CTGF was studied by MTT. Results CTGF could stimulate fibroblasts proliferation with a dose-dependant manner, and activa-ted the ERK1/2 signal pathway, and AI built up to 0.209±0.0201, reaching the apex at 15 min after stimulation performed. Inhibition of ERK1/2 activation by PD98059 suppressed CTGF-mediated HS fi-broblasts proliferation significantly, while OD significantly dropped. Conclusion CTGF induces a prolif-erative response in HS fibroblasts, and this action is mainly dependent on the activation of ERK1/2 signal pathway.