蛇床子素对博莱霉素致肺纤维化小鼠的干预作用及其机制研究

Effects of Osthole on Mice with Pulmonary Fibrosis Induced by Bleomycin

摘要: 目的：观察蛇床子素(Osthole, Ost)对博莱霉素(BLM)致小鼠肺纤维化的干预作用及可能的作用机制。方法：小鼠随机分为对照组、模型组、醋酸泼尼松组和Ost大、中、小剂量组。BLM气管内给药复制小鼠肺纤维化模型，于造模成功后第2天各治疗组Ost灌胃给药，给药后第28天处死小鼠，观察肺组织形态学变化，并测定肺纤维化相关生化指标。结果：Ost能减少BLM致肺纤维化小鼠肺组织中胶原沉积，降低肺系数(P < 0.05)，增强肺组织及血清中总抗氧化能力(T-AOC)及增强其抑制羟自由基(•OH)能力，降低肺组织中羟脯氨酸(HYP)及丙二醛(MDA)含量，减弱肺血清中总一氧化氮合酶的活力(T-NOS) (P < 0.05, P<0.01, P < 0.001)，减轻小鼠肺组织纤维化改变。结论：Ost对BLM诱导肺纤维化有一定程度的干预与治疗作用。

Abstract: Objective: To observe the intervention effect and possible mechanism of phylogenetic fibrosis in mice caused by bleomycin (BLM) by Osthole (Ost). Methods: Mice were randomly divided into con-trol group, modal group, prednisone acetate group and Ost large, medium and small dose group. BLM endotracheal administration replicated the mouse pulmonary fibrosis model, and on the sec-ond day after successful molding, each treatment group was gastrically administered Ost, and the mice were sacrificed on the 28th day after administration, and the morphological changes of lung tissue were observed, and the biochemical indicators related to pulmonary fibrosis were measured. Results: Ost can reduce collagen deposition in lung tissue of BLM-induced pulmonary fibrosis mice, reduce lung coefficient (P < 0.05), enhance total antioxidant capacity (T-AOC) in lung tissue and se-rum, and enhance its inhibition of hydroxyl radicals (•OH) ability, reduce the content of hydroxypro-line (HYP) and malondialdehyde (MDA) in lung tissue, weaken the activity of total nitric oxide syn-thase (T-NOS) in lung serum (P < 0.05, P < 0.01, P < 0.001), and reduce the fibrosis changes in mouse lung tissue. Conclusion: Ost has a certain degree of intervention and therapeutic effect on BLM-induced pulmonary fibrosis.