目的：探讨吡菲尼酮对牛血清蛋白诱导的大鼠肝纤维化的影响。方法雄性Wistar大鼠30只被随机分为3组，给予模型组腹腔注射牛血清白蛋白，正常对照组接受等量的生理盐水腹腔注射,治疗组在腹腔注射牛血清白蛋白5 w后，按200 mg·kg-1·d-1灌胃给药吡菲尼酮，治疗4 w后处死试验动物，留取肝脏组织，行HE和Mas-son染色，观察肝脏病理学改变，采用免疫组化法检测Smad6蛋白表达。结果与模型组比，吡菲尼酮治疗组肝组织纤维化S3和S4期病变较模型组明显减少，炎症细胞浸润明显减少，胶原纤维间隔缩小，着色变浅；模型组肝组织Smad6相对表达量为（108.2±33.6），显著低于吡菲尼酮治疗组[（329.4±39.2），P<0.05]。结论吡菲尼酮可抑制牛血清蛋白诱导的大鼠肝纤维化，其机制与通过上调Smad 6蛋白表达有关。%Objective To investigate the impact of pirfenidone on liver fibrosis induced by bovine serum albumin (BSA) in rats and its relevant mechanism. Methods 30 male Wistar rats were randomly divided into three groups: e.g. in control group the rats were given saline intraperitoneally,in model group were given BSA intraperitoneally,and in treatment group were given intragastric administration of pirfenidone at the dose of 200 mg.kg-1.d-1 after 5-week intraperitoneal injection of BSA. The animals were sacrificed after 4-week treatment and the liver specimens were collected. Hepatic pathology was per-formed by haematoxylin-eosin stain and Masson trichrome stain ,and the expression of Smad 6 was detected by immunohisto-chemistry. Results As compared with in model group,the number of cases with liver fibrosis stage of S3-S4 in treatment group decreased,with significantly reduced infiltration of inflammatory cells,narrowed fibrous septum in liver tissues. Relative expression of Smad 6 in model group was significantly lower than that in treatment group [(108.2±33.6) vs. (329.4±39.2), P<0.05]. Conclusions Pirfenidone can inhibit liver fibrosis induced by BSA in rats,which might be attributed to the upreg-ulation of Smad 6.
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