【摘要】 目的探讨一氧化氮(NO)在CCl4致大鼠肝纤维化中的作用。方法Wistar大鼠34只,雄性,体重200~220g,用CCl4制造大鼠肝纤维化模型,另设正常对照组大鼠6只。HE染色、Massons染色,观察肝组织病理学改变;检测血清NO,肝组织丙二醛(MDA)、超氧化物歧化酶(SOD)。结果肝纤维化模型组大鼠第7周达到2期或3期肝纤维化,汇管区周围纤维隔形成并相互连接,部分纤维隔深入小叶内,小叶结构保留或紊乱,但无肝硬化,伴有中度脂肪变性及肝细胞空泡变性;血清NO水平明显增高(152·8±12·30μmol/Lvs.11·03±1·95μmol/L,P<0·05),肝组织MDA含量明显增高(2·11±0·26nmol/mgprotvs.0·73±0·13nmol/mgprot,P<0·05),SOD活性明显降低(44·96±5·36nU/mgprotvs.105·73±13·5nU/mgprot,P<0·05)。结论随着大鼠肝纤维化的形成,大鼠血清NO水平随之增高,进一步导致肝细胞炎症及损伤,促进了肝纤维化的形成。更多还原

【Abstract】 Objective To explore the oxidation stress effects of nitrogen monoxide （NO） on rats’ hepatic fibrosis induced by carbon tetrachloride （CCl₄）. Methods Thirty-four male Wistar rats were subcutaneously given CCl₄ to induce hepatic fibrosis model. Six additional rats were chosen to serve as control group. Histological sections of liver of the animals were stained by H & E and Massons staining. NO in serum, malon-dialdehyde （MDA） and superoxide dismutase （SOD） in liver tissue were determined. Results At 7th week, grade 2 or 3 of hepatic fibrosis was reproduced, in which fibrous tissue formed fibrous septa, around the portal areas stretching into hepatic lobules. The structure of the hepatic lobules was intact or disarranged, but there was no signs of cirrhosis. There was moderate fatty change and vacuolar degeneration of heputocytes. The level of serum NO increased significantly （152.8±12.30μmol/L vs. 11.03±1.95μmol/L, P<0.05）. The content of MDA increased significantly in the homogenate of hepatic tissue （2.11±0.26nmol/mg vs. 0.73±0.13nmol/mg prot, P<0.05）, while SOD decreased significantly （44.96±5.36nU/mg prot vs. 105.73±13.5nU/mg prot, P<0.05）. Conclusion The results suggest that in the process of fibrosis in the liver, serum level of NO gradually elevated, further aggravating inflammation and injury to liver cells, thus promotes hepatic fibrosis.更多还原