Magnesium Sulfate Attenuates Lipopolysaccharides-Induced Acute Lung Injury in Mice
Magnesium Sulfate Attenuates Lipopolysaccharides-Induced Acute Lung Injury in Mice
复制标题
硫酸镁减轻脂多糖引起的小鼠急性肺损伤
DOI：
10.4103/cjp.cjp_48_19
复制
发表时间：
2019-09-01
影响因子：
1.8
通讯作者：
Wang, Yujiong
中科院分区：
文献类型：
--
作者：
Li, Wu;Wu, Xiaoling;Wang, Yujiong
急性肺损伤（acute lung injury，ALI）是一种常见的严重呼吸系统疾病，发病率和死亡率都很高.尽管近年来取得了一些进展，但对ALI的发病机制仍知之甚少，治疗效果仍未得到明显改善。众所周知，硫酸镁（MgSO 4）具有有效的抗炎能力。本研究旨在探讨MgSO 4对脂多糖（LPS）诱导的ALI的保护作用。本研究采用昆明种小鼠尾静脉注射内毒素（LPS）建立急性肺损伤（ALI）模型，同时采用A549细胞建立细胞模型。检测肺湿/干重比、肺组织丙二醛（MDA）含量、肺通透性指数、苏木精-伊红染色、血清和支气管肺泡灌洗液（BALF）中细胞因子、BALF中中性粒细胞计数、LPS诱导的A549细胞凋亡以及小鼠和A549细胞中凋亡诱导因子（AIF）和多聚腺苷二磷酸核糖聚合酶-1（PARP-1）的表达。我们的研究结果表明，硫酸镁显着减弱LPS诱导的ALI，氧化应激（降低MDA水平），和肺部炎症反应。MgSO 4通过减轻LPS诱导的A549细胞凋亡而发挥保护作用。此外，MgSO 4在体内和体外均降低AIF和PARP-1的表达。考虑到硫酸镁在临床环境中的常用性，我们的结果表明硫酸镁是一种潜在的治疗急性肺损伤的药物。
Acute lung injury (ALI) is a common and severe respiratory disease with high morbidity and mortality. Although some progress has been made in the past years, the pathogenesis of ALI is still poorly understood and the therapeutic outcome has still not been significantly improved. It is well-recognized that magnesium sulfate (MgSO4) possesses potent anti-inflammation capacity. The present study was designed to investigate the protective effects of MgSO4 in lipopolysaccharides (LPSs)-induced ALI taken into account that excessive inflammatory response plays critical role in the development of ALI. In this study, Kunming mice were intravenously injected with LPS through tail vein to establish the ALI model and in parallel, A549 cells were used to establish cell model. The lung wet-to-dry weight ratio, malondialdehyde (MDA) levels in lung tissue, lung permeability index, hematoxylin and eosin staining, cytokines in the serum and bronchoalveolar lavage fluid (BALF), neutrophil counts in BALF, LPS-induced A549 cell apoptosis as well as apoptosis-inducing factor (AIF), and Poly(ADP-ribose) polymerase-1 (PARP-1) expression in both mice and A549 cells were detected. Our results demonstrated that MgSO4 significantly attenuated the LPS-induced ALI, oxidative stress (decreased MDA levels), and lung inflammatory response. Moreover, MgSO4 exerted protective effects by mitigating LPS-induced A549 cell apoptosis. Furthermore, MgSO4 decreased the AIF and PARP-1 expression both in vivo and in vitro. Our results, taken together, demonstrated that MgSO4 is a potential therapeutic agent for ALI taken into consideration that MgSO4 is commonly used in clinical settings.