黄芩总黄酮对博莱霉素致大鼠肺纤维化的干预作用及其机制研究

Influence of total flavonoids from Scutellaria baicalensis on Bleomycin-induced pulmonary fibrosis in rats and its mechanism

目的观察黄芩总黄酮对博莱霉素致大鼠肺纤维化的影响及其作用机制。方法 SD大鼠随机分为5组:对照组、模型组、泼尼松龙阳性对照(3.34 mg/kg)组、黄芩总黄酮高剂量和低剂量(50、25 mg/kg)组。大鼠气管内注射博莱霉素制备肺纤维化模型后,各给药组ig给予相应药物,每天给药1次。28 d后处死动物,观察大鼠血清中总抗氧化能力(T-AOC)、还原性谷胱甘肽(GSH)、髓过氧化物酶(MPO)的水平;取固定部位肺组织分别行HE、Masson染色,进行病理组织学检查;RT-PCR法检测黄芩总黄酮对大鼠肺组织中TGF-β1、Smad2、Smad7、α-SMA、胶原I的mRNA表达水平。结果与模型组相比,黄芩总黄酮给药组大鼠血清中T-AOC、GSH水平均升高,MPO水平显著降低;肺泡炎和肺纤维化程度明显减轻(P<0.05、0.01);TGF-β1、Smad2、α-SMA、胶原I基因表达显著降低,Smad7表达显著升高(P<0.05、0.01)。结论黄芩总黄酮对博莱霉素所致大鼠肺纤维化具有一定的治疗作用,其机制可能与抗氧化损伤、抑制炎症细胞的浸润活化及调控TGF-β1/Smad信号通路有关。

Objective To observe the influence of total flavonoids from Scutellaria baicalensis（TFSB） on Bleomycin-induced pulmonary fibrosis in rats and investigate the relative mechanism.Methods The pulmonary fibrosis model was established by intratracheal injection of Bleomycin.After 28 d,rats with TFSB treatment by ig administration once a day were killed.The levels of T-AOC,GSH,and MPO in serum were measured and analyzed and the fixed parts of the lung tissue were obtained for HE and Masson staining for histopathological examination.The influences of TFSB on the expression of transforming growth factor-β1（TGF-β1）,Smad2,Smad7,α-SMA,and Collagen I mRNA in lung tissue of rats with Bleomycin-induced pulmonary fibrosis were assayed by RT-PCR.Results Compared with the model group,the levels of T-AOC and GSH in serum were dramatically increased and the level of MPO was decreased remarkably after TFSB treatment;The alveolitis and fibrosis extent were attenuated after TFSB treatment（P 〈0.05,0.01）,and the expression levels of TGF-β1,Smad2,α-SMA,and Collagen I mRNA were decreased,and the expression level of Smad7 mRNA was increased（P〈0.05,0.01） significantly.Conclusion TFSB could have mitigable effect on Bleomycin-induced pulmonary fibrosis in rats.The mechanisms might be related to the anti-oxidative damage,the inhibition of activation of inflammatory cell infiltration,and the regulation of TGF-β1/Smad signal pathway.