Apocynin ameliorates endotoxin-induced acute lung injury in rats
Apocynin ameliorates endotoxin-induced acute lung injury in rats
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DOI：
10.1016/j.intimp.2015.12.006
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发表时间：
2016-01-01
影响因子：
5.6
通讯作者：
Suddek, Ghada M.
中科院分区：
文献类型：
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作者：
Abdelmageed, Marwa E.;El-Awady, Mohammed S.;Suddek, Ghada M.
急性肺损伤（ALI）是一种严重的临床综合征，死亡率很高。在本研究中，研究了夹竹桃麻素（一种 NADPH 氧化酶 (NOX) 抑制剂）对脂多糖 (LPS) 诱导的大鼠 ALI 的影响。雄性 Sprague-Dawley 大鼠在注射 LPS（10 mg/kg，i.p.）前 1 小时腹膜内（i.p.）用罗布麻素（10 mg/kg）治疗。结果显示，罗布麻宁可减轻LPS诱导的ALI，因为它降低了总蛋白含量、乳酸脱氢酶（LDH）活性和支气管肺泡灌洗液（BALF）中炎症细胞的积累，此外，与LPS组相比，罗布麻宁显着增加了超氧化物歧化酶（SOD）并降低了谷胱甘肽（GSH）活性，同时肺组织中的丙二醛（MDA）含量显着降低。减少LPS引起的肺动脉收缩。它还上调抑制蛋白 kappaB-alpha (NF kappa Bia) 的 mRNA 表达，下调 Toll 样受体 4 (TLR4) 的 mRNA 表达，并减少肺组织中观察到的炎症。总的来说，这些结果证明了罗布麻宁通过其抗氧化和抗炎作用对大鼠中 LPS 诱导的 ALI 具有保护作用，这可能归因于 TLR4 mRNA 表达的减少和 NF kappa Bia mRNA 表达的增加。 (C) 2015 Elsevier B.V. 保留所有权利。
Acute lung injury (ALI) is a serious clinical syndrome with a high rate of mortality. In this study, the effects of apocynin, a NADPH-oxidase (NOX) inhibitor on lipopolysaccharide (LPS)-induced ALI in rats were investigated. Male Sprague-Dawley rats were treated with apocynin (10 mg/kg) intraperitoneally (i.p.) 1 h before LPS injection (10 mg/kg, i.p.). The results revealed that apocynin attenuated LPS-induced ALI as it decreased total protein content, lactate dehydrogenase (LDH) activity and the accumulation of the inflammatory cells in the bronchoalveolar lavage fluid (BALF), In addition, apocynin significantly increased superoxide dismutase (SOD) and reduced glutathione (GSH) activities with significant decrease in the lung malondialdehyde (MDA) content as compared to LPS group in lung tissue and decreased pulmonary artery contraction induced by LPS. It also up regulated mRNA expression of inhibitory protein kappaB-alpha (NF kappa Bia) and downregulated mRNA expression of Toll-Like receptor 4 (TLR4) and decreased inflammation observed in lung tissues. Collectively, these results demonstrate the protective effects of apocynin against the LPS-induced ALI in rats through its antioxidant and antiinflammatory effect that may be attributed to the decrease in mRNA expression of TLR4 and increasing that of NF kappa Bia. (C) 2015 Elsevier B.V. All rights reserved.