摘要
背景:肝星状细胞的激活、增殖导致肝纤维化,p38丝裂原活化蛋白激酶信号通路可参与调控细胞增殖。目的:探讨SB203580作用于乙醛刺激的大鼠肝星状细胞后p38丝裂原活化蛋白激酶活性变化和细胞增殖变化。方法:体外培养大鼠肝星状细胞株,在乙醛干预的基础上加入不同浓度的p38特异性抑制剂SB203580进行培养,并设置对照。以Westernblot检测磷酸化p38蛋白表达水平变化,MTT比色法检测细胞增殖。结果与结论:乙醛刺激后大鼠肝星状细胞内磷酸化p38水平增强,细胞增殖明显。使用5,10,20μmol/L SB203580能明显抑制乙醛刺激的肝星状细胞增殖(P<0.05),加大浓度至30μmol/L时,抑制作用更明显(P<0.01),抑制率为43.9%,而磷酸化p38水平也降低(P<0.05)。结果证实,抑制p38丝裂原活化蛋白激酶活性可能影响肝星状细胞的增殖。
BACKGROUND：Activation and proliferation of hepatic stellate cells （HSCs） leads to hepatic fibrosis,and p38 mitogen-activated protein kinase （p38MAPK） signaling pathway has a role in regulating cell proliferation.OBJECTIVE：To explore the p38MAPK activity and cell proliferation of acetaldehyde-induced rat HSCs treated with SB203580.METHODS：Rat HSC strains were cultured in vitro,and divided into blank group,acetaldehyde control group and SB203580 group.The proliferation of HSCs was evaluated by MTT colorimetric assay and the variability of phosphorylated-p38 was examined by Western blot.RESULTS AND CONCLUSION：p38 activity increased in acetaldehyde-induced HSCs,and HSCs proliferated significantly;SB203580 （5,10,20μmol/L） could block the activity of p38 in the cells,and inhibit acetaldehyde-induced HSCs proliferation （P〈0.05）,when the concentration was increased to 30μmol/L,its inhibitive effect on HSCs proliferation was more significant,and the expression of p-p38 decreased relatively （P〈0.05）.The results showed that inhibition of p38MAPK activity can affect HSCs proliferation;p38 signaling pathway may play an important role in the regulation of HSCs proliferation.
出处
《中国组织工程研究与临床康复》
CAS
CSCD
北大核心
2011年第20期3711-3714,共4页
Journal of Clinical Rehabilitative Tissue Engineering Research
