摘要
目的探讨核酸在CCl4诱导的肝纤维化模型中对肝脏中M1型乙酰胆碱受体的影响及其抗肝纤维化的可能机制。方法应用四氯化碳(CCl4)诱导大鼠慢性肝纤维化模型。将55只Wistar大鼠分为4组:正常对照(N)组10只?肝复乐胶囊对照(G)组15只?核酸(Z)组15只及模型(M)组15只。采用光镜观察肝组织病理学改变;运用免疫组织SP法?逆转录聚合酶链反应(RT-PCR)和Western-blot方法检测各组肝组织M1型胆碱能受体(M1-AChR)不同水平的表达情况。结果核酸组、肝复乐胶囊对照组病理改变较模型组明显改善;免疫组织化学?RT-PCR?Western-blot三种不同层次水平的表达结果均表明核酸组和肝复乐胶囊对照组M1-AChR的表达较模型组显著降低(P<0.05)。结论核酸可降低肝纤维化肝组织中M1型乙酰胆碱受体的含量,可能主要通过调节肝纤维化大鼠肝脏中的M1型乙酰胆碱受体的含量而达到抗肝纤维化的作用。
Objective To investigate the effect of nucleic acid on M1-acetylcholine receptor and the possible mechanism resisting hepatic fibrosis induced by carbon tetrachloride （CCl4 ）. Methods The rats were divided randomly into four groups： normal control （n = 10）, Ganfule （n = 15）, nucleic acid （n = 15 ）, and model （n = 15）. The pathological histology of the liver was observed by HE staining. We used immunohistochemistry, RT- PCR and Western-blot to measure the expression of M1 acetylcholine receptors in the liver tissue. Results Compared with that of the model group, the liver histology of the nucleic acid group was improved significantly. The results of immunohistochemistry, RT-PCR and Western-blot all showed decreased expression in the nucleic acid group and the Gan fule group compared with that in the model group, the difference being significant （ P 〈 0. 05 ）. Conclusion Nucleic acid can decrease the concentration M1-acetylcholine receptors in liver tissue of fibrosis, and inhibit the hepatic fibrosis mainly by regulating the levels of M1-acetylcholine receptor in rats with hepatic fibrosis.
出处
《中国组织化学与细胞化学杂志》
CAS
CSCD
2008年第1期95-99,共5页
Chinese Journal of Histochemistry and Cytochemistry
关键词
核酸
M1型胆碱能受体
肝纤维化
Nucleic acid
M 1 -acetylcholine receptor
Liver fibrosis
