论文部分内容阅读
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 effect of total flavonoids from Scutellaria baicalensis Georgi on pulmonary fibrosis induced by bleomycin and its mechanism. Methods SD rats were randomly divided into 5 groups: control group, model group, prednisolone positive control (3.34 mg / kg) group, Scutellaria total flavonoids high dose and low dose (50, 25 mg / kg) group. After intratracheal injection of bleomycin in rats to prepare pulmonary fibrosis model, each administration group ig given corresponding drugs, administered once a day. After 28 days, the animals were sacrificed to observe the levels of total antioxidant capacity (T-AOC), glutathione (GSH) and myeloperoxidase (MPO) in the serum of the rats. , Masson staining and histopathological examination. The mRNA expression of TGF-β1, Smad2, Smad7, α-SMA and collagen I of Scutellaria baicalensis Georgi was detected by RT-PCR. Results Compared with the model group, the levels of T-AOC and GSH in the serum of rats treated with Scutellaria total flavonoids were significantly increased, and the levels of MPO were significantly decreased. The levels of alveolitis and pulmonary fibrosis were significantly reduced (P <0.05, 0.01) β1, Smad2, α-SMA, collagen I gene expression was significantly reduced, Smad7 expression was significantly increased (P <0.05,0.01). Conclusion Scutellaria total flavonoids may play a therapeutic role in bleomycin-induced pulmonary fibrosis in rats. The mechanism may be related to anti-oxidative damage, inhibiting infiltration and activation of inflammatory cells and regulating TGF-β1 / Smad signaling pathway.