黑木耳多糖对内毒素诱导急性肺损伤大鼠肺组织的保护作用

摘要

目的：探讨黑木耳多糖对LPS诱导急性肺损伤大鼠肺组织的保护作用及其机制。方法：将健康SD大鼠随机分为对照组、LPS组、地塞米松组以及黑木耳多糖低、中、高浓度组，根据分组，分别给予生理盐水或不同浓度黑木耳多糖预防性灌胃7 d，第8天腹腔注射生理盐水或LPS（8 mg／kg），地塞米松组在给予LPS后腹腔注射地塞米松（3 mg／kg）。造模12 h后于腹主动脉取血，并制肺组织匀浆和肺泡灌洗液。检测支气管肺泡灌洗液中蛋白含量、肺湿／干重比、髓过氧化物酶（MPO）、总抗氧化能力（T－AOC）、总超氧化物歧化酶（T－SOD）、一氧化氮合酶（ NOS）、丙二醛（ MDA）等指标，做组织切片HE染色并进行肺损伤评分。结果：应用黑木耳多糖干预后，急性肺损伤大鼠支气管肺泡灌洗液中蛋白含量明显下降，肺湿／干重比值降低；大鼠肺组织中MPO、NOS活性及MDA含量较LPS组降低，T－AOC含量和T－SOD活性较之升高；肺组织病理改变减轻，肺损伤指数下降。结论：黑木耳多糖具有保护LPS损伤大鼠肺组织的作用，其机制可能与其抗氧化作用有关。%AIM:To investigate the effects of Auricularia auricular-judae polysaccharide ( AAP) on pulmonary tissues of rats with LPS-induced acute lung injury (ALI) and its mechanisms.METHODS: Adult Sprague-Dawley rats were randomly divided into control group , LPS group, low-dose AAP group, middle-dose AAP group, high-dose APP group, and dexamethasone group.The rats were injected with LPS (8 mg/kg, ip) to induce ALI.The rats in the AAP groups were treated with AAP for 7 d before the induction of ALI .The protein concentration in the bronchoalveolar lavage fluid (BALF) was measured.The lung edema degree was measured by detecting the wet /dry weight ratio.The myeloper-oxidase ( MPO) , total antioxidant capacity ( T-AOC) , total superoxide dismutase ( T-SOD) , nitric oxide synthase ( NOS) and malondialdehyde ( MDA) levels were determined .The pathological changes of the lung tissues were evaluated by HE staining.RESULTS:Treatment with AAP significantly improved LPS-induced lung pathological changes , attenuated the protein concentration in the BALF and wet/dry weight ratio , inhibited the activities of MPO and NOS , reduced MDA level and increased the activities of T-AOC and T-SOD.CONCLUSION: AAP protects against LPS-induced acute lung injury in rats.