扶正理气合剂抗酒精性肝纤维化的实验研究

Experimental research on anti-fibrosis effect of Fuzheng-Liqi mixture in rat hepatic fobrosis induced by alcohol

目的 探讨复方中药扶正理气合剂对洒精性肝纤维化的预防机制和效果.方法 雄性SD大鼠80只,随机分为正常组、模型组、复方丹参组和扶正理气合剂组.以乙醇灌胃诱导大鼠肝纤维化模型,复方丹参组造模同时给予复方丹参灌胃,扶正理气合剂组造模同时给予扶正理气合剂灌胃,共16周.16周后处死大鼠取肝组织标本,光镜观察肝组织的病理变化,放射免疫法测定血清丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性.结果 ①模型组多数正常小叶结构破坏或消失,由汇管区和中央静脉伸出粗大胶原纤维条索分割肝小叶,肝细胞索排列紊乱,肝细胞明显水肿,广泛脂肪变性.纤维隔内有大量淋巴细胞、单核细胞、嗜酸性粒细胞等浸润.与模型组比较,两个用药组肝小叶结构破坏明显减轻,肝脏胶原纤维增生亦明显减轻,纤维条索疏松变窄.肝细胞水肿好转,炎细胞浸润减少.②Masson染色胶原纤维面积比较：模型组胶原面积比正常组显著增加（P＜0.05）,复方丹参组和扶正理气合剂组胶原面积较模型组均减轻（P＜0.05）,扶正理气合剂组与复方丹参组比较无显著差异（P＞0.05）.③与模型组比较,复方丹参组、扶正理气合剂组MDA下降（P＜0.01）、SOD升高（P＜0.05）.结论 扶正理气合剂抗纤维化作用可能与其抗脂质过氧化作用有关.

Objective To explore the mechanisms and preventive effects of Fuzheng-Liqi mixture on alcoholic hepatic fibrosis. Methods 48 male SD rats were randomly divided into four groups： normal group, model group, Compound Salviae Miltiorrhizae （CSM） group and Fuzheng-Liqi mixture （FLM） group. Alcohol was poured into stomach of the rats for 16 weeks to induce hepatic fibrosis. At the same time, CSM and FLM were given to each group. The rats were killed after 16 weeks. Histomorphylogic structure of the liver tissues was observed under optical microscope; the levels of MDA and SOD in rounded by thick cords of collagen fibers, which extended from the portal areas and central veins. Obvious cloudy swelling could be seen in hepatocytes. Fatty degeneration was extensive, and some with necroses fiber septa were infiltrated by a great number of cells such as monocytes, lymphocytes, eosinophilic granulocytes, fibroblasts, and so on. Compared with the model group, the destructions were slighter, proliferations of collagen fibers were also fewer, fiber cords were more loosened and comparison of collagen area in Masson staining： The collagen area in the CSM group and FLM group were less than the model of serum SOD was increased obviously in the FLM group （P＜0.05）. Conclusion The mechanism of Fuzheng-Liqi mixture in anti-fibrosis effects may be correlated with its anti-lipid peroxidation.