蒙古扁桃种仁不同极性部位对博来霉素致大鼠肺纤维化的保护作用

Protective Effect of Different Polar Parts of Amygdalus mongolica on Pulmonary Fibrosis Rat Models Induced by Bleomycin

目的:观察蒙古扁桃药材不同极性部位对博来霉素致大鼠肺纤维化的影响。方法:通过气管内注射博来霉素建立肺纤维化大鼠模型,给予蒙古扁桃治疗后,HE、Masson染色评估肺组织病理变化及检测肺组织中超氧化物歧化酶(superoxide dismutase,SOD)和丙二醛(malondialdehyde,MDA)含量,检测肺组织中TGF-β1、Smad3和α-SMA通路蛋白表达,观察蒙古扁桃不同极性部位对博来霉素致大鼠肺纤维化形成影响。结果:与模型组比较,石油醚、正丁醇部位提取物可显著(P<0.05)降低肺纤维化小鼠肺指数,显著(P<0.05)升高肺组织SOD活性,减轻小鼠肺泡炎和肺纤维化程度,并显著(P<0.05)降低肺组织中MDA、肺组织中TGF-β1、Smad 3和α-SMA mRNA的表达。结论:蒙古扁桃药材四种活性部位中,石油醚、正丁醇部位提取物是对博来霉素致大鼠肺纤维化具有较好保护作用的活性部位。机制是通过清除活性氧抵抗脂质过氧化作用,下调Smad 3,抑制TGF-β1和α-SMA的表达发挥抗肺纤维化的作用。

Objective:This study aimed to investigate the effect of different polarities of Amygdalus mongolica on pulmonary fibrosis induced by bleomycin in rats.Methods:The rat model of pulmonary fibrosis was established by intratracheal injection of bleomycin.Then the rat was treated with Amygdalus mongolica.The pathological changes of lung tissues were detected by using HE stain and Masson’s trichrome stain,and the contents of superoxide dismutase(SOD)and malondialdehyde(MDA)in lung tissues were measured.In addition,the expression of TGF-β1,Smad3 andα-SMA protein in lung tissue was detected to observe the effect of different polarities of Amygdalus mongolica on pulmonary fibrosis induced by bleomycin in rats.Results:Compared with the model group,extracts from petroleum ether and n-butanol of Amygdalus mongolica significantly decreased the indexes of pulmonary fibrosis(P<0.05),significantly increased the activity of SOD in lung tissue(P<0.05),reduced the alveolar inflammation and pulmonary fibrosis(P<0.05),and significantly decreased the expression of MDA,TGF-β1,Smad3 andα-SMA mRNA in lung tissue(P<0.05).Conclusion:Of the four active components of Amygdalus mongolica,the extracts of petroleum ether and n-butanol produce a good protective effect on pulmonary fibrosis induced by bleomycin in rats.The mechanism is that Smad3 downregulated and TGF-β1 andα-SMA are inhibited by scavenging reactive oxygen species against lipid peroxidation,so as to produce effect against pulmonary fibrosis.