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目的探讨姜黄素对体外培养大鼠肝星状细胞细胞株(CSFSC-2G)增殖能力及细胞外基质分泌的影响。方法四甲基偶氮噻唑蓝(MTT)法检测不同浓度姜黄素(5,10,15,20,40μmol/L)在不同培养时间作用下肝星状细胞(HSC)的增殖能力;酶联免疫吸附实验法检测不同浓度姜黄素作用下HSCI型胶原(CollagenI,ColI)和III型胶原(CollagenIII,ColIII)合成及分泌能力;流式细胞术检测姜黄素对HSC凋亡的影响。结果不同浓度的姜黄素(5,10,15,20,40μmol/L)均可抑制HSC增殖,并呈现明显剂量依赖关系;含20μmol/L姜黄素培养基培养24h后,HSC-ColI、ColIII吸光度(A)值分别为(0.418±0.019),(0.554±0.043),均明显低于阴性对照组,差异有统计学意义(P<0.05);含20μmol/L姜黄素培养基培养48h后,HSC处于G0/G1期的HSC细胞占(39.98±8.07)%,S期细胞占(55.79±9.13)%,G2/M期细胞占(4.23±0.12)%;凋亡率为(20.31±2.55)%,高于阴性对照组凋亡率(0.22±0.11)%,低于秋水仙素阳性药物对照组凋亡率(29.75±2.64)%,差异均有统计学意义(P<0.05)。结论姜黄素可抑制HSC细胞的增殖并促进其凋亡,有可能成为防治肝纤维化的理想药物。
Objective To investigate the effect of curcumin on the proliferation and extracellular matrix secretion of cultured rat hepatic stellate cell line (CSFSC-2G) in vitro. Methods MTT assay was used to detect the proliferation of hepatic stellate cells (HSC) with different concentrations of curcumin (5, 10, 15, 20 and 40 μmol / L) The synthesis and secretion of HSCI collagen (CollagenI, ColI) and collagen III (CollagenIII, ColIII) under different concentrations of curcumin were detected by adsorption assay. The effect of curcumin on the apoptosis of HSC was detected by flow cytometry. Results Curcumin at different concentrations (5, 10, 15, 20 and 40 μmol / L) inhibited HSC proliferation in a dose-dependent manner. After cultured with 20 μmol / L curcumin for 24 h, HSC-ColI and ColIII absorbance (A) values were (0.418 ± 0.019) and (0.554 ± 0.043), respectively, which were significantly lower than those in the negative control group (P <0.05). After cultured with 20μmol / L curcumin for 48h, The percentage of HSC cells in G0 / G1 phase was (39.98 ± 8.07)%, in S phase cells was (55.79 ± 9.13)%, in G2 / M phase cells was (4.23 ± 0.12)%, in apoptotic cells was (20.31 ± 2.55) , Which was higher than that of the negative control group (0.22 ± 0.11)%, which was lower than that of the colchicine positive control group (29.75 ± 2.64)%, the differences were statistically significant (P <0.05). Conclusion Curcumin can inhibit the proliferation of HSC cells and promote its apoptosis, which may become an ideal drug for prevention and treatment of hepatic fibrosis.