卡维地洛对肝纤维化模型大鼠肝组织瘦素及瘦素受体表达的影响

发布时间：2018-06-18 07:29

本文选题：肝纤维化 + 大鼠　；参考：《山东医药》2015年22期

【摘要】：目的探讨卡维地洛抑制肝纤维化的效果及机制。方法将36只雄性SD大鼠随机分为对照组6只、模型组10只、治疗1组及治疗2组各10只。模型组和治疗组采用胆总管结扎法建立大鼠肝纤维化模型。治疗1、2组造模成功后48 h开始每天予卡维地洛药液1 mg/kg分2次灌胃,分别用药2、4周;对照组及模型组同时灌等量蒸馏水。实验结束后取各组大鼠肝左叶组织切片,行常规HE染色和Masson三色染色,光镜下观察各组肝脏纤维化情况;Western blot法检测各组肝组织瘦素以及瘦素受体表达;Real-time Q-PCR法检测瘦素及瘦素受体mRNA。结果 HE及Masson三色染色光镜下观察可见,模型组成功建立胆汁淤积性肝纤维化模型,随着造模时间延长肝纤维化程度逐渐加重。治疗1、2组肝脏纤维化程度较模型组减轻,肝脏纤维化分期降低,P0.05。治疗2组肝纤维化程度与治疗1组无统计学差异(P0.05)。模型组肝组织瘦素、瘦素受体蛋白及mRNA表达量均较对照组升高(P均0.05),治疗1、2组肝组织瘦素、瘦素受体蛋白及mRNA表达量均较模型组降低(P均0.05),两治疗组相比无统计学差异(P0.05)。结论卡维地洛能对肝纤维化有抑制作用;其机制可能为下调瘦素及瘦素受体基因表达。
[Abstract]:Objective to investigate the effect and mechanism of carvedilol on hepatic fibrosis. Methods 36 male SD rats were randomly divided into control group (n = 6), model group (n = 10), treatment group (n = 10) and treatment group (n = 10). Model group and treatment group were used to establish hepatic fibrosis model by common bile duct ligation. Carvedilol was given orally for 1 mg/kg for 2 weeks, and the control group and the model group were given the same amount of distilled water at the same time. At the end of the experiment, the liver Zuo Ye sections of each group were taken and stained by routine HE staining and Masson trichrome staining. The liver fibrosis in each group was observed under light microscope. Leptin and leptin receptor expression in liver tissue were detected by Western blot method and real-time Q-PCR for detection of leptin and leptin receptor mRNA. Results HE and Masson trichrome staining showed that the model group successfully established the model of cholestatic liver fibrosis, and the degree of hepatic fibrosis gradually increased with the prolongation of the time of modeling. Compared with the model group, the degree of hepatic fibrosis in treatment group 1 and 2 was reduced, and the stage of hepatic fibrosis was decreased (P 0. 05). There was no significant difference in the degree of hepatic fibrosis between the treatment group and the treatment group (P 0.05). The expression of leptin, leptin receptor protein and mRNA in the model group was higher than that in the control group (P < 0.05). The expression of leptin, leptin receptor protein and mRNA in the liver tissue in the treatment group was lower than that in the model group (P < 0.05), and there was no significant difference between the two groups (P 0.05). Conclusion Carvedilol can inhibit hepatic fibrosis by down-regulating leptin and leptin receptor gene expression.
【作者单位】：河北省人民医院;
【分类号】：R575.2

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