三七总皂甙对大鼠体内肝卵圆细胞增殖的作用

Effects of panax notoginoside saponins on the proliferation of rat hepatic oval cells in vivo

目的研究三七总皂甙(PNS)对大鼠体内肝卵圆细胞(HOC)增殖的影响。方法选择体重150g左右的雄性Wistar大鼠,随机分为对照组、模型组和PNS组。采用2-AAF/PH方法建立HOC增殖模型。常规组织学检查,OV-6、AFP及CK19免疫组化鉴定HOC,并观察PNS腹内注射后HOC增殖的变化。结果对照组肝小叶、肝窦结构清晰,无增生反应。模型组和PNS组肝索结构紊乱,肝细胞坏死,汇管区伴有增生反应。与模型组比较PNS组肝组织破坏轻,恢复快,增生反应轻;模型组4d汇管区有明显HOC增殖反应,8d HOC增殖达峰值。PNS组各时间点HOC增殖显著少于模型组(P<0.05),12d HOC增殖达峰值。结论大鼠2-AAF/PH是理想的HOC增殖模型;PNS可调节体内HOC的增殖过程,使HOC增殖峰降低、持续时间延长。

Objective To investigate the effects of panax notoginoside saponins （PNS） on the proliferation of rat hepatic oval cell. Methods Male wistar rats （weight about 150g） were randomly divided into three groups： the control group, the model group, and the PNS group. The rat model for hepatic oval cells proliferation was established by 2 - AAF/PH protocol. The morphological changes were observed by hematoxylin and eosin （HE） staining, and OV -6, AFP and CK19 were detected to identify HOC proliferation by immunohistochemical staining. The changes of hepatic oval cells proliferation in the PNS （with intraperitoneal PNS） groups were observed. Results Histopathological changes of rats liver were normal and there was no proliferation in rats liver in the control group, while hepatocytic necrosis, distortion of hepatic architecture and proliferation at portal area were the prominent features in rats liver of the model group and the PNS group. However, the damage of hepatic architecture and HOC proliferation were slighter in the PNS group than that in the model group. HOC proliferation was obvious on the 4th day and increased to the peak on the 8th day in the model group. HOC proliferation was slighter on the corresponding day in the PNS group that that in the model group （P 〈 0.05）, and HOC proliferation in-creased to the peak on the 12th day in the PNS group. Conclusion Ideal rat model for hepatic oval cells proliferation can be obtained by 2AAF/PH protocol. PNS can regulate the process of hepatic oval ceils proliferation in vivo through deereasing the peak and prolonging duration of HOC proliferation.