目的 探讨咖啡因(CAF)对乙醛刺激的大鼠肝星状细胞(HSC)-T6增殖、凋亡的影响及部分作用机制.方法用不同浓度的CAF(0.5、1、2、4、8 mmol/L)对乙醛刺激的HSC-T6进行处理,四甲基偶氮唑蓝(MTT)法检测细胞增殖;流式细胞仪检测细胞凋亡及细胞周期分布;RT-PCR法检测HSC-T6中平滑肌肌动蛋白(α-SMA)、肿瘤坏死因子相关凋亡诱导配体(TRAIL)受体DR4、DR5的mRNA表达.结果 CAF对乙醛刺激的大鼠HSC-T6增殖具有抑制作用,阻滞细胞于G0/G1期;能够明显下调HSC-T6中α-SMA的mRNA表达,上调DR4、DR5的mRNA表达.结论 CAF对乙醛刺激的HSC-T6增殖具有抑制作用,并能够促进其凋亡,其机制可能与TRAIL受体DR4、DR5的表达有关.%Objective To explore the effect of caffeine on proliferation, apoptosis in hepatic stellate cell-T6( HSCT6 ) stimulated by acetaldehyde and its partial mechanisms. Methods HSC-T6 stimulated by acetaldehyde was incubated with different doses of caffeine( 0. 5 ,1 .2 ,4 ,8 mmol/L ) , cell proliferation was analyzed by MTT colorimetric assay, apoptosis rate and the cell cycle distribution were analyzed by flow cytometry( FCM ). The mRNA expressions of a-SMA.TRAIL receptor DR4 and DR5 were measured by RT-PCR. Results Caffeine could inhibit HSCT6 stimulated by acetaldehyde,the cells were accumulated in the G0/G1 phase. The mRNA expression levels of αSMA decreased,but DR4 and DR5 increased. Conclusion Caffeine can inhibit the growth of HSC-T6 stimulated by acetaldehyde and promote the apoptosis,the mechanisms may be related to the expression of TRAIL receptor DR4 and DR5.
展开▼
