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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,其作用机制与抑制脂质过氧化反应及Hsc活化响关
Objective: To study the preventive effect of anti-fibrosis compound I (KXI) on alcoholic liver disease and its mechanism by using a rat model of alcoholic liver disease. 2. Methods: A rat model of alcoholic liver disease was prepared by ethanol gavage. Wistar rats were randomly divided into 3 groups, normal group, alcohol group and Chinese medicine group. At the same time, the Chinese medicine group was given anti-fibrosis compound I decoction (crude drug concentration 4.5kg/L) 4mL/kg-1, 2 Times / d gavage, observation 12wk. At the end of 4wk, 8wk and 12wk, the animals were sacrificed in batches. HE and VG staining were used to observe the hepatocyte degeneration and fibrous tissue proliferation in each group. Semi-quantitative analysis of fibrous tissue proliferation was performed using pathological image analyzer. The morphological changes of hepatic stellate cells were observed under electron microscope. The content of malondialdehyde (MDA) in liver tissue of rats in each group was determined by TBA colorimetric method, and the content of superoxide dismutase (SOD) was measured by hydroxylamine method. Results: At the end of 4wk of HE stained alcohol group, hepatocyte necrosis, steatosis, and inflammatory cell infiltration were observed. At the end of 12wk, the number of steatosis and hepatocyte necrosis increased. The Chinese medicine group only appeared mild steatosis at 8wk, and hepatocyte necrosis and inflammatory cell infiltration were not obvious. In the VG-stained alcohol group, fibrous tissue hyperplasia was seen, which showed a cord-like extension into the hepatic lobule. The Chinese medicine group had no fiber ties. Collagen area percentage of alcohol in the image analyzer was significantly higher in the alcohol group than in the normal group and the Chinese medicine group (19.24±2.5 vs 4.6±0.7, 19.24±2.5 vs 9±0.9, P<0.05. ). Under electron microscope, the liver cells in the alcohol group lost their normal structures, astrocytes were increased and deformed, and more collagen fibrils were observed outside the cells. The morphology of hepatocytes and astrocytes in the traditional Chinese medicine group was basically normal, and a small amount of collagen fibrils was also found in the matrix. MDA in alcohol group had increased at the end of 4wk, which was significantly different from that in normal group and Chinese medicine group (32±3vs16±7, 32±3vs23±8, P<0.05). Conclusion The second anti-fibrosis compound I has good The role of anti-rat alcoholic liver disease, its mechanism of action and suppression of lipid peroxidation and Hsc activation