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目的 探讨核糖体S6激酶(RSK)在大鼠肝纤维化发生中的作用。方法 采用腹腔注射二甲基亚硝胺的方法构建大鼠实验性肝纤维化模型。以免疫荧光双标记 激光扫描共聚焦显微镜成像技术检测RSK与α-平滑肌肌动蛋白(α- SMA)及Ⅰ型胶原。进一步利用免疫组化法检测 RSK与Ⅰ、Ⅲ型胶原在肝纤维化组织中的表达及其相关性。结果 在纤维化肝组织中,RSK的定位与α-SMA完全一致,Ⅰ型胶原伴随RSK周围分布。RSK与Ⅰ、Ⅲ型胶原的表达量之间亦呈显著相关(P<0.05)。结论 肝纤维化发生中,RSK定位于活化的肝星状细胞内,并参与胶原的表达调控。RSK可能成为治疗肝纤维化的新靶点。
Objective To investigate the role of ribosomal S6 kinase (RSK) in the pathogenesis of hepatic fibrosis in rats. Methods The rat experimental hepatic fibrosis model was established by intraperitoneal injection of dimethylnitrosamine. The expressions of RSK, α-SMA and collagen Ⅰ were detected by immunofluorescence double labeling laser confocal microscopy. Further use of immunohistochemistry to detect the expression of RSK and type Ⅰ, Ⅲ collagen in hepatic fibrosis and its correlation. Results The localization of RSK in fibrotic liver tissue was completely consistent with that of α-SMA. Type I collagen was distributed around RSK. There was also a significant correlation between the expression of RSK and type Ⅰ and type Ⅲ collagen (P <0.05). Conclusion RSK is localized in activated hepatic stellate cells in the pathogenesis of hepatic fibrosis and is involved in the regulation of collagen expression. RSK may be a new target for the treatment of liver fibrosis.