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[目的]研究姜黄素抑制大鼠肝星状细胞(HSC)活化作用与过氧化物酶体增殖因子活化受体γ(PPARγ)信号转导途径之间的关系。[方法]肝脏原位灌流酶消化、Nycodenz密度梯度离心方法分离培养大鼠HSC,并使用姜黄素对细胞进行相应处理,采用四甲基偶氮唑蓝(MTT)比色分析法检测姜黄素对细胞增殖的影响。收集裂解细胞并抽提细胞总RNA,采用半定量RT-PCR检测姜黄素处理对α平滑肌肌动蛋白(-αSMA)和Ⅰ型胶原的基因表达水平的影响。[结果]姜黄素在10~50μmol/L范围内呈剂量依赖性抑制体外培养大鼠传代HSC的增殖,且能在基因水平显著降低-αSMA(P<0.05)和I型胶原的基因表达水平(P<0.01)。这些作用均可以被PPARγ特异性阻断剂GW9662阻断。[结论]姜黄素抑制HSC增殖、活化和合成I型胶原的作用依赖于PPARγ信号转导途径的激活。
[Objective] To study the relationship between curcumin-induced activation of rat hepatic stellate cells (HSC) and peroxisome proliferator-activated receptor gamma (PPARγ) signal transduction pathway. [Methods] Liver in situ enzyme digestion and Nycodenz density gradient centrifugation were used to isolate and culture rat HSCs. The cells were treated with curcumin and MTT colorimetric assay was used to detect curcumin. Effect of cell proliferation. The lysed cells were collected and total cellular RNA was extracted. The effects of curcumin treatment on the gene expression levels of α-smooth muscle actin (-αSMA) and type I collagen were detected by semi-quantitative RT-PCR. [Results] Curcumin inhibited the proliferation of rat HSCs cultured in vitro in a dose-dependent manner in the range of 10 to 50 μmol/L, and it could significantly reduce the level of α-SMA (P<0.05) and type I collagen gene expression at the gene level ( P<0.01). Both of these effects can be blocked by the PPARγ-specific blocker GW9662. [Conclusion] The curcumin inhibited HSC proliferation, activation and synthesis of type I collagen depended on the activation of PPARγ signal transduction pathway.