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首页> 外文期刊>Microbial Pathogenesis >Alpha-linolenic acid protects against lipopolysaccharide-induced acute lung injury through anti-inflammatory and anti-oxidative pathways
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Alpha-linolenic acid protects against lipopolysaccharide-induced acute lung injury through anti-inflammatory and anti-oxidative pathways

机译：α-亚麻酸通过抗炎和抗氧化途径免受脂多糖诱导的急性肺损伤

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摘要

Alpha-linolenic acid (ALA), an important component of polyunsaturated fatty acids (PUFAs), possesses potent anti-inflammatory properties. To date, the effects of ALA on acute lung injury (ALI) remains unknown. This study was designed to investigate the potential protective effects of ALA on LPS-induced ALI and the underpinning mechanisms. An animal model of ALI was established via intratracheally injection of lipopolysaccharide (LPS, 1 mg/kg). We found that lung wet/dry weight ratio and protein concentration in Bronchoalveolar lavage fluid (BALF) were dramatically decreased by ALA pretreatment. Treatment with ALA significantly alleviated the infiltration of total cells and neutrophils, while increased the number of the macrophages. ALA significantly inhibited the secretion of proinflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and interleukin-1 beta (IL-1 beta) and increased anti-inflammatory cytokine. Moreover, we found that the levels of myeloperoxidase (MPO) and malondialdehyde (MDA) were highly increased in LPS-induced ALI, while the activities of glutathione (GSH) and superoxide dismutase (SOD) were decreased, which were reversed by ALA. ALA attenuated LPS-induced histopathological changes and apoptosis. Furthermore, ALA significantly inhibited the phosphorylation of I kappa B alpha and NF-kappa B (p65) activation in ALI. ALA showed anti-inflammatory effects in mice with LPS-induced ALI. NF-kappa B pathway may be involved in ALA mediated protective effects.
机译：α-亚麻酸（ALA）是多不饱和脂肪酸（PUFAs）的重要组成部分具有效率的抗炎特性。迄今为止，ALA对急性肺损伤（ALI）的影响仍然未知。本研究旨在探讨ALA对LPS诱导的ALI和支撑机制的潜在保护作用。通过腹腔内注射脂多糖（LPS，1mg / kg）建立ALI的动物模型。我们发现，ALA预处理，支气管肺泡灌洗液（BALF）中的肺湿/干重比和蛋白质浓度显着降低。用ALA治疗显着缓解了总细胞和中性粒细胞的渗透，同时增加了巨噬细胞的数量。 ALA显着抑制促炎细胞因子的分泌，包括肿瘤坏死因子-α（TNF-α），白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）和增加的抗炎细胞因子。此外，我们发现髓氧化酶（MPO）和丙二醛（MDA）的水平在LPS诱导的ALI中高度增加，而谷胱甘肽（GSH）和超氧化物歧化酶（SOD）的活性降低，其被ALA逆转。 ALA衰减LPS诱导的组织病理学变化和细胞凋亡。此外，ALA显着抑制ALI中κBα和NF-Kappa B（P65）活化的磷酸化。 ALA表现出具有LPS诱导的Ali的小鼠的抗炎作用。 NF-Kappa B途径可参与ALA介导的保护作用。

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