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目的:研究复方六月青(CLYQ)对四氯化碳(CCl4)致肝纤维化大鼠肝组织Ⅰ型胶原(Col I)合成的抑制作用。方法:SD大鼠sc CCl4建立肝纤维化模型,随机分为5组:模型对照组、秋水仙碱组、CLYQ高剂量组、中剂量组、低剂量组,并设正常SD大鼠为空白对照组。模型组和空白对照组ig生理盐水,其他组ig相应的药物,连续4周。采用实时荧光定量PCR法检测各组肝组织Col I mRNA表达情况,采用免疫组织化学法检测各组肝组织Col I蛋白表达情况。结果:与模型对照组比,CLYQ各剂量组大鼠肝组织Col I mRNA的表达均下调(P<0.01),且表现一定的剂量依赖性;CLYQ各剂量组大鼠肝组织Col I蛋白阳性表达面积和强度显著减少和减弱(P<0.01或P<0.05),且呈明显的剂量依赖性。结论:CLYQ可下调肝纤维化大鼠肝组织Col I mRNA表达及其蛋白质合成以抑制细胞外基质的沉积,从而发挥其抗肝纤维化的作用。
Objective: To study the inhibitory effect of CLYQ on the synthesis of collagen Ⅰ (Col I) in hepatic fibrosis rats induced by carbon tetrachloride (CCl4). Methods: The hepatic fibrosis models were established by sc CCl4 in SD rats. They were randomly divided into 5 groups: model control group, colchicine group, CLYQ high dose group, middle dose group and low dose group, and normal SD rats as blank control group. The model group and blank control group ig saline, the other group ig the corresponding drug for 4 weeks. The expression of Col I mRNA in each group was detected by real-time fluorescence quantitative PCR. The expression of Col I in each group was detected by immunohistochemistry. Results: Compared with the model control group, the expression of Col I mRNA in liver tissue of CLYQ groups was down-regulated (P <0.01), and showed a dose-dependent manner. The expression of Col I protein in each group of CLYQ Area and intensity significantly reduced and weakened (P <0.01 or P <0.05), and showed a significant dose-dependent. CONCLUSION: CLYQ can down-regulate the expression of Col I mRNA in liver tissue and its protein synthesis to inhibit the deposition of extracellular matrix, thereby exerting its anti-hepatic fibrosis effect.