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目的建立维吾尔医异常黑胆质型肝癌病证大鼠模型,探讨信号转导及转录活化因子3(STAT3)基因在异常黑胆质型肝癌病证发生发展中的作用及意义。方法利用异常黑胆质证造模法及二乙基亚硝胺诱导建立异常黑胆质型肝癌病证模型组、肝癌对照组,同时设立正常对照组。应用半定量PCR(RT-PCR)检测各组肝脏组织中STAT3基因的mRNA水平的表达,免疫组织化学SP法和蛋白免疫印记法(Western blot)检测各组肝脏组织中STAT3基因的蛋白水平的表达。结果肝癌对照组与正常对照组相比,STAT3基因的mRNA水平明显上调,差异有统计学意义(P<0.01),异常黑胆质型肝癌病证模型组与肝癌对照组相比,STAT3基因的mRNA水平明显上调,差异有统计学意义(P<0.01)。免疫组化SP法及Western blot结果显示肝癌对照组STAT3蛋白表达水平高于正常对照组,差异有统计学意义(P<0.01),异常黑胆质型肝癌病证模型组STAT3蛋白表达水平高于肝癌对照组,差异有统计学意义(P<0.05)。结论在异常黑胆质型肝癌的发生过程中,二乙基亚硝胺(DEN)是肝癌发生的主要原因,异常黑胆质体液起了促进作用。异常黑胆质体液可能通过对STAT3肝癌基因的影响,促进异常黑胆质型肝癌的发生、发展。
Objective To establish a rat model of abnormal savda hepatocarcinoma with Uyghur medicine and to explore the role and significance of signal transducer and activator of transcription 3 (STAT3) gene in the pathogenesis of abnormal savda hepatobaroma. Methods Abnormal savda syndrome model and diethylnitrosamine induced model of abnormal Savda hepatocarcinoma model and control group of hepatocellular carcinoma were established. At the same time, a normal control group was established. The expression of STAT3 mRNA in liver tissues of each group was detected by semi-quantitative PCR (RT-PCR). The expression of STAT3 gene protein in liver tissues of each group was detected by immunohistochemical SP method and Western blot . Results Compared with the normal control group, the mRNA expression of STAT3 in hepatocellular carcinoma control group was significantly increased (P <0.01). Compared with the control group, the expression of STAT3 gene in the model group of abnormal savda hepatocellular carcinoma mRNA level was significantly increased, the difference was statistically significant (P <0.01). Immunohistochemical SP method and Western blot results showed that the expression of STAT3 protein in hepatocellular carcinoma control group was higher than that in normal control group (P <0.01), and the expression of STAT3 protein in abnormal savda hepatocarcinoma model group was higher than Liver cancer control group, the difference was statistically significant (P <0.05). Conclusion Diethylnitrosamine (DEN) is the main cause of hepatocellular carcinoma in the process of abnormal savda hepatoblasts, and abnormal savda body fluid plays a promoting role. Abnormal Savda humoral fluid may promote the occurrence and development of abnormal savda hepatocarcinoma by affecting the STAT3 hepatocellular carcinoma gene.