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目的通过分析癌痛消方(AP)干预二乙基亚硝胺(DEN)诱癌大鼠模型在不同时间点的肝脏组织病理变化、细胞凋亡的相关蛋白表达变化,来探讨癌痛消方治疗原发性肝癌的机制。方法将50只♂Wistar大鼠随机分为预防组、模型组(每组20只)和空白对照组(10只),预防组和模型组的大鼠以64 ppm DEN饮水饲养,连续16周。同时,自诱癌之日起,预防组大鼠予以AP灌胃0.2 g·(100 g)~(-1),qd,每周连续用药6 d,给药周期为18周;模型与空白对照组正常饮食,饮水(自来水)。分别在4、8、12、16、18周时,随机各取预防组和模型组的4只大鼠、2只空白对照组的,断颈处死,取肝组织(阳性部位)免疫组化法检测Bax、Bcl-2、survivin、Fas、Fasl、caspase-3蛋白的表达情况。结果空白对照组未见survivin、casepase-3、Fas/Fasl、Bax、Bcl-2蛋白的表达;模型组各时间点均可见凋亡相关蛋白的表达,以凋亡抑制蛋白Bcl-2、survivin表达量较多;AP干预过程可以全程下调survivin、Bcl-2蛋白的表达,上调Fas、casepase、Bax蛋白的表达。结论 AP可以促进受损肝细胞或癌细胞凋亡,其预防和治疗肝癌机理是上调促凋亡蛋白、下调抑凋亡蛋白的表达,促进炎症细胞或肿瘤细胞凋亡。
OBJECTIVE: To investigate the effects of Jia Tong Xiao Prescription (AP) on the pathological changes of liver tissue and the expression of apoptosis-related proteins at different time points in rats induced by diethylnitrosamine (DEN) Mechanism of treatment of primary liver cancer. Methods Fifty male Wistar rats were randomly divided into prophylaxis group, model group (n = 20) and blank control group (n = 10). Rats in prevention group and model group were fed with 64 ppm DEN water for 16 weeks. At the same time, the rats in the prophylaxis group were given intragastrically 0.2 g · (100 g) -1 of AP for qd administration for 6 days per week for 6 weeks, and the administration period was 18 weeks. The model and blank control Group normal diet, drinking water (tap water). At 4, 8, 12, 16 and 18 weeks, 4 rats in prevention group and model group were randomly selected. Two rabbits in blank control group were sacrificed and their liver tissues (positive) immunohistochemical method The expression of Bax, Bcl-2, survivin, Fas, Fasl and caspase-3 protein were detected. Results The expression of survivin, casepase-3, Fas / Fasl, Bax and Bcl-2 protein were not found in the blank control group. The expression of apoptosis-related protein Bcl-2 and survivin AP intervention could down-regulate the expression of survivin and Bcl-2 protein and up-regulate the expression of Fas, casepase and Bax. Conclusion AP can promote the apoptosis of damaged hepatocytes or cancer cells. The mechanism of prevention and treatment of hepatocellular carcinoma is to up-regulate pro-apoptotic proteins, down-regulate anti-apoptotic proteins and promote the apoptosis of inflammatory cells or tumor cells.