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目的 观察石荠芋总黄酮(MSF)对博来霉素致大鼠肺纤维化的干预作用,并初步探讨其机制.方法 60只SD大鼠随机分为正常组,模型组,阳性对照组,MSF低、中、高剂量组,气道注射博来霉素(5 mg·kg-1)制备大鼠肺纤维化模型.造模14d后,阳性对照组给予2 mg·kg-1醋酸泼尼松,MSF低、中、高剂量组分别给予40,80,160 mg·kg-1,正常组和模型组给予等量生理盐水,每天1次,连续28d,于造模42 d后检测血清超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、白细胞介素-4(IL-4)、肿瘤坏死因子-α(TNF-α)、转化生长因子-β1(TGF-β1)和透明质酸(HA)含量,Masson染色观察纤维化发展情况,免疫组化检测α-肌动蛋白(α-SMA)表达,蛋白印迹检测核因子-κB(NF-KB)、TGF-β1、TNF-α、Smad2/3和pSmad2/3表达情况.结果 与模型组相比,MSF干预后大鼠血清SOD、GSH活性显著增加;IL-4、TNF-α、TGF-β1和HA含量显著降低(P＜0.01);α-SMA表达明显下调,纤维化程度减轻;NF-κB、TNF-α、TGF-β1、Smad2/3和pSmad2/3表达显著降低(P＜0.01).结论 MSF对肺纤维化具有一定的治疗作用,其机制可能与抑制NF-KB和TGF-β1通路信号转导有关.“,”OBJECTIVE To investigate protective effects of total flavonoids from Mosla scabra(MSF) on bleomycininduced pulmonary fibrosis of rats,and explore its preliminary mechanism.METHODS Sixty SD rats were divided into six groups randomly:normal group,model group,positive control group,MSF high-dose,middle-dose and low-dose treatment group.Pulmonary fibrosis in rats was induced by intratracheal instillation of belomycin (5 mg·kg-1).After challenge of 14 d,the two treatment groups were given MSF at the doses of 40,80 and 160 mg·kg 1 respectively,while positive control group was treated with prednisone acetate (2 mg.kg-1).Normal group and model group were treated with saline once a day for 28 d.The activities of SOD and GSH,the levels of IL-4,TNF-α,TGF-β1 and HA in serum were detected after molding 42 d.The histological examination was performed with Masson stain.The expression of α-SMA was detected by immunohistochemistry analysis while the expression of NF-κB,TNF-α,TGF-β1,Smad2/3 and pSmad2/3 proteins was detected by Western-blotting analysis.RESULTS Compared with the model group,the activities of SOD and GSH were increased significantly whereas levels of IL-4,TNF-α,TGF-β1 and HA in serum were decreased significantly after MSF treatment (P＜0.01).The expression of α-SMA was down-regulated.The degree of fibrosis was reduced.The protein expressions of NF-κB,TNF-α,TGF-β1,Smad2/3 and pSmad2/3 were also significantly decreased (P＜0.01).CONCLUSION MSF can ameliorate pulmonary fibrosis through inhibition of NF-κB and TGF-β1 signaling.