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目的探讨胆汁酸如何通过调控肝星状细胞促进肝纤维化发生。方法采用BrdU掺入法测定胆汁酸和TGFβ-1对GFSC-2G细胞增殖的影响;利用Wound-healing检测法判定细胞的移动能力;同时利用Western blotting法检测与胆汁酸共同孵育的GFSC-2G细胞的p38和JNK的表达。结果与50μmol/L甘氨鹅脱氧胆酸(GCDCA)共同孵育后,CFSC-2G细胞增殖明显增加,为对照组的152.0%±7.1%(P<0.05)。50μmol/L GCDCA诱导p38及JNK磷酸化的作用[在p38为对照组的450.0%±12.2%(P<0.01),在JNK为对照组的210.0%±15.2%(P<0.05)]。50μmol/L GCDCA促进培养细胞的伤痕愈合(剩余面积为原来的75.4%±5.8%,P<0.05),而JNK(SP600125)或p38(SB294002)的抑制因子能够抑制胆汁酸的这种作用。结论胆汁酸具有促进肝星状细胞增殖的作用,还能提高该细胞的运动能力,这种作用是通过促进p38和JNK的磷酸化而实现的。提示胆汁酸可能通过调控p38和JNK的信号转导而促进肝纤维化的形成。
Objective To investigate how bile acid can promote hepatic fibrosis by regulating hepatic stellate cells. Methods BrdU incorporation method was used to determine the effect of bile acid and TGFβ-1 on the proliferation of GFSC-2G cells. Wound-healing assay was used to determine the cell migration ability. GFSC-2G cells co-incubated with bile acid The expression of p38 and JNK. Results After incubation with 50 μmol / L GDC, the proliferation of CFSC-2G cells was significantly increased, which was 152.0% ± 7.1% of the control group (P <0.05). The effect of pCD and JNK phosphorylation induced by 50 μmol / L GCDCA [at p38 was 450.0% ± 12.2% (P <0.01) in control group and 210.0% ± 15.2% (P <0.05) in JNK control group. Fifty micromol / L GCDCA promoted wound healing in cultured cells (remaining area was 75.4% ± 5.8% of the original, P <0.05), whereas inhibitors of JNK (SP600125) or p38 (SB294002) inhibited this effect of bile acids. Conclusion Bile acid can promote the proliferation of hepatic stellate cells and increase the motility of the cells. This effect can be achieved by promoting the phosphorylation of p38 and JNK. It is suggested that bile acids may promote the formation of hepatic fibrosis by regulating the signal transduction of p38 and JNK.