三七总皂甙对大鼠肝卵圆细胞增殖肝脏CX/GJIC的影响

Effect of PNS on the Expression of CX/GJIC in Rat Liver for Hepatic Oval Cell Proliferation

目的研究三七总皂甙(Panax notoginoside,PNS)对大鼠肝卵圆细胞增殖模型肝脏缝隙连接蛋白(con-nexin,CX)表达及其介导的缝隙连接细胞间通讯(gap junction intercellular communication,GJIC)的影响。方法选择体重150 g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(2-acetylamin-ofluorene+two thirds partial hepatectomy)建立肝卵圆细胞增殖模型,切开标记/染料示踪技术(incision loading/dye transfer,IL/DT)检测肝脏GJIC,免疫组织化学法检测CX32、43的表达和计数肝卵圆细胞,并观察PNS腹内注射后的表达变化。结果(1)对照组未见肝卵圆细胞,PNS组、模型组肝卵圆细胞增殖明显;PNS组与模型组相比,卵圆细胞增殖高峰低、持续时间长。(2)各组CX32和GJIC的表达:模型组与PNS组均低于对照组,表达峰呈先下调后逐渐恢复趋势,PNS组高于模型组。(3)各组CX43的表达:模型组与PNS组均高于对照组,表达峰呈先升高后逐渐恢复与肝卵圆细胞的增殖趋势一致,PNS组与模型组相比表达高峰滞后。结论2-AAF/PH是理想的肝卵圆细胞增殖模型;CX32和GJIC的下调可动员肝卵圆细胞,CX43可促进其增殖,CX/GJIC对肝卵圆细胞增殖有重要的调控作用;PNS可通过影响CX/GJIC的表达,调节肝卵圆细胞的增殖过程。

Objective To investigate the effect of PNS on the expression of CX/GJIC in the rat liver during 2-Acetylaminofluorene/Partial Hepatectomy for hepatic oval cells proliferation. Methods Male wistar rats （weight about 150g） were randomly divided into three groups： control group, model group,and PNS group. A rat model was established for hepatic oval cells proliferation using 2-AAF/PH protocol. The expression of CX32,CX43 and the proliferation of hepatic oval cells were detected with immunohistochemical. GJIC was analyzed with IL/DT. The rats in PNS group were intraperitoneal injected with PNS. Results （1）The proliferation of hepatic oval cells was obvious in both PNS and model groups,but absent in control group. Compared to the model group, the peaks of hepatic oval cells proliferation were lower and postponed to later days in PNS group. （2） Expression levels of CX32 and GJIC were lower in both PNS and model groups than that in control group which presented reverse tendency of hepatic oval cells proliferation, but was higher in PNS group than that in PNS and model groups were higher than that model group. （3）The expression levels of CX43 in in control group. Compared to model group, the peaks of PNS group were postponed to later days presented similar tendency of hepatic oval cells proliferation. Conclusion Satisfactory rat models for hepatic oval cells proliferation can be obtain using 2AAF/PH protocol. Hepatic oval cells were activated by the decrease expression of CX32 and GJIC. Hepatic oval cells proliferation can be promoted by CX43 expression. The process of hepatic oval cells proliferation can be regulated by CX/GJIC which was influenced by PNS.