摘要
目的以秋水仙碱为对照药物,观察温阳中药复方肝之福预防实验性肝纤维化形成的病理组织学作用,并初步探讨其作用机制。方法Wistar大鼠45只随机分为4组:正常对照组、肝之福组、秋水仙碱组及模型对照组。除正常组外,其余3组均采用CCl4SC及饮用100ml/L乙醇的方法制备大鼠肝纤维化模型。在造模的同时,肝之福组予肝之福灌胃,秋水仙碱组予秋水仙碱灌胃,模型对照组予等量生理盐水灌胃,1次/d,共30d。实验结束后取肝组织测定羟脯氨酸(Hyp)含量、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性,并根据炎症活动度及纤维化半定量计分系统(SSS)评分,观察预防用药组与模型对照组的组织学变化,同时对肝组织内Ⅰ、Ⅲ、Ⅳ型胶原进行染色并定量分析。结果与模型对照组相比,肝之福组Hyp含量由(1.52±0.35)mg/g减少到(1.12±0.29)mg/g(P<0.05),MDA含量由(16.3±6.0)μmol/g减少到(8.8±2.1)μmol/g(P<0.01),而SOD活性则由(86.33±17.74)nkat/g升高至(122.01±19.12)nkat/g(P<0.01);同时,SSS评分炎症活动度及肝纤维化程度明显改善,肝组织内Ⅰ型、Ⅲ型、Ⅳ型胶原含量下降。经比较,肝之福抗肝纤维化的上述疗效与秋水仙碱相当。结论肝之福可预防实验性肝纤维化的形成,抗脂质过氧化是其可能的作用机制。
Objective To observe the preventive pathological effect of Ganzhifu on the course of experimental hepatic fibrosis accompanied with colchicine as control and to explore the initial mechanism. Methods Fifty-nine Wistar rats were used in this study comprising four groups： normal group, Ganzhifu group, colchicine group and model group. Except normal group, the other three groups were given subcutaneous injection of CCL4 and drinking 10% alcohol so as to make the model of hepatic fibrosis. At the same time the rats of Ganzhifu group were given the herbal remedies via gastric canal once each day, the rats of colchicine group were given colchicine group by same way, the rats of model group were given normal saline. At the end of the experiment,hydroxyproline （Hyp） eontent,malondial dehyde （MDA） content, superoxide disumutase （SOD） activity of liver tissue were measured respectively. Tissue microarray sections of liver were stained with HE, Masson and Gorden-Sweet to observe pathological changes and calculate the point according to inflammation and fibrosis semiquantative scoring system （SSS） of liver tissue. In addition, immunohistochemistry examinations were done to observe the expression of Ⅰ ,Ⅲ , Ⅳ type collagen and the content of each type collagen were analysed with computer. Results Compared with model group,liver function is improved remarkably, and there was a notable decline of liver fibrosis marks, Hyp content reduced from （1.52±0.35） mg/g to （1.12±0.29） mg/g （P〈0.05） and MDA content from （16.3±6.0）μmol/g to （8.8±2.1）μmol/g （P〈 0.01 ） accompany with a striking rise of SOD activity from （86/33±17.74） nkat/g to （ 122.01±19.12） nkat/g （ P 〈 0.01 ） .Pathological findings and collagen content analysis showed that the Ganzhifu group had less inflammation, lower degree fibrosis and reduced content of Ⅰ , Ⅲ , Ⅳ type collagen than model group. The effect of Ganzhifu on liver fibrosis was parallel with colchicine. Conclusion Ganzhifu can prevent the experimentals hepatic fibrosis. The possible mechanism of Ganzhifu is antioxidation.
出处
《四川医学》
CAS
2005年第10期1062-1065,共4页
Sichuan Medical Journal
基金
四川省卫生厅科研基金资助(No:F0196)
