机构地区:[1]中国医科大学第一临床学院消化内科,辽宁省沈阳市110001 [2]中国医科大学第一临床学院肾病实验室,辽宁省沈阳市110001
出 处:《世界华人消化杂志》2002年第11期1245-1249,共5页World Chinese Journal of Digestology
摘 要:目的:利用酒精性肝病的大鼠模型,研究抗纤复方Ⅰ号(KXI)对酒精性肝病的预防作用及其机制.方法:采用乙醇灌胃法制备酒精性肝病大鼠模型.Wistar大鼠随机分为3组,正常组,酒精组及中药组.中药组在造模同时,给予抗纤复方Ⅰ号水煎剂(生药浓度4.5kg/L)4mL/kg-1,2次/d灌胃,观察12wk.实验4wk、8wk、12wk末分批处死动物,HE及VG染色观察各组大鼠肝细胞变性及纤维组织增生情况,应用病理图像分析仪对纤维组织增生进行半定量分析.电镜下观察肝星形细胞形态改变.应用TBA比色法测定各组大鼠肝组织中丙二醛(MDA)含量,羟胺法测定超氧化物歧化酶(SOD)含量.结果:HE染色酒精组4wk末即出现肝细胞坏死,脂肪变,炎性细胞浸润.12wk末脂肪变及肝细胞坏死增多,中药组8wk时才出现轻度脂肪变,肝细胞坏死及炎性细胞浸润均不明显.VG染色酒精组可见纤维组织增生,呈条索状向肝小叶内延伸,中药组无纤维条索形成.图像分析仪所示胶原面积百分比酒精组明显高于正常组及中药组(19.24±2.5vs4.6±0.7,19.24±2.5vs9±0.9,P<0.05).电镜下观察酒精组肝细胞失去正常结构,星形细胞增多、变形,细胞外可见较多胶原原纤维.中药组肝细胞及星形细胞形态基本正常,基质内亦可见少量胶原原纤维.酒精组MDA在实验4wk末即已升高,与正常组及中药组比较差异显著(32±3vs16±7,32±3vs23±8,P<0.05),结论二抗纤复方I号具有良好的抗大鼠酒精性肝病的作用。AIM:To investigated the effect of Kang Xian Fu Fang I(KXI) on fibrogenesis in ethanol-induced liver disease in the rats and its mechanisms.METHODS:Wistar rats weighing between 160 and 200 g were used to establish alcohol-induced liver disease model as previously described. Medicine-treated rats were administrated KXI (4 ml · kg-1 · d-1) twice a day plus equal etha-nol with ethanol-fed rats for 12 wk. Rats were killed at the end of 4 wk, 8 wk and 12 wk. H-E and V-G stains were used to evaluate liver histopathological alterations. Ultrastructural changes were detected by electron microscope. Liver MDA and SOD were measured by chemical methods.RESULTS:In ethanol-fed rats, slight steatosis and spotty hepatocellular necrosis were observed after 4 weeks. Up to 12 weeks, marked hepatic fatty changes, inflammation, necrosis and mild fibrosis were also observed. In contrast, these alterations were attenuated by KXI administration although mild fatty changes remained. Semi quantity analysis showed the rates of collagen to hepatic areas were significantly increased in alcohol-fed group than those in normal and medicine-treated rats (19.24 F± 2.5 vs 4.6 ± 0.7, 19.24 ± 2.5 vs 9 ± 0.9, P<0.05). Ultrastructural observation showed that hepatocytes lost normal formation, and hepatic stellate cells (HSC) increased and became myofibroblast-like cells and there was a large of collagen around cells in ethanol-fed rats. In medicine-treated rats, hepatocytes and hepatic stellate cells remained normal shape and only a little of collagen was observed. Liver MDA significantly increased at the fourth week in alcohol-fed groupcompared with control and medicine-treated groups (32 ± 3 vs 16 ± 7, 32 ± 3 vs 23 ± 8, P < 0.05). With time of etha-nol exposure, liver MDA increased gradually (32 ± 3 →36 ± 4 → 62 ± 2, P<0.05). Ethanol admission caused an increase in liver SOD and there were no significantly differences among the alcohol-fed and medicine-treated rats at the end of 4 weeks. However, SOD decreased gradually in the alcoh
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