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姜烯酮通过Akt-NFκB信号通路减轻内毒素诱导的急性肺损伤小鼠的炎症反应。

Zerumbone reduced the inflammatory response of acute lung injury in endotoxin-treated mice via Akt-NFκB pathway.

作者信息

Ho Yung-Chyuan, Lee Shiuan-Shinn, Yang Ming-Ling, Huang-Liu Rosa, Lee Chien-Ying, Li Yi-Ching, Kuan Yu-Hsiang

机构信息

School of Medical Applied Chemistry, Chung Shan Medical University, Taichung, Taiwan.

School of Public Health, Chung Shan Medical University, Taichung, Taiwan.

出版信息

Chem Biol Interact. 2017 Jun 1;271:9-14. doi: 10.1016/j.cbi.2017.04.017. Epub 2017 Apr 22.

Abstract

Zerumbone, a cyclic eleven-membered sesquiterpene, is the major component of the essential oil isolated from the wild ginger, Zingiber zerumbet. There are several beneficial pharmacological activities of zerumbone including anti-inflammatory, antioxidant, and anticancer activities. Acute lung injury (ALI) is an acute pulmonary inflammatory disorder with high morbidity and mortality rate. In present study, we aimed to investigate the protective effects and mechanisms of zerumbone on endotoxin, lipopolysaccharide (LPS)-induced ALI. Mice were pretreated with zerumbone at various concentrations for 30 min followed by intratracheal administration of LPS for 6 h. Pretreatment with zerumbone not only reduced leukocytes infiltration into the alveolar space but also inhibited lung edema in LPS-induced ALI. Decreased secretion of proinflammatory cytokines such as TNFα and IL-6 caused by LPS were reversed by zerumbone. LPS-induced expressions of proinflammatory mediators, iNOS and COX-2, were inhibited by zerumbone. In addition, NFκB activation and Akt phosphorylation were inhibited by zerumbone in LPS-induced ALI. All these results suggested that the protective mechanisms of zerumbone on endotoxin-induced ALI were via inhibition of Akt-NFκB activation.

摘要

姜酮醇是一种环状十一元倍半萜,是从野生姜黄姜中分离出的挥发油的主要成分。姜酮醇具有多种有益的药理活性,包括抗炎、抗氧化和抗癌活性。急性肺损伤(ALI)是一种发病率和死亡率都很高的急性肺部炎症性疾病。在本研究中,我们旨在探讨姜酮醇对内毒素、脂多糖(LPS)诱导的ALI的保护作用及其机制。用不同浓度的姜酮醇预处理小鼠30分钟,然后气管内给予LPS 6小时。姜酮醇预处理不仅减少了白细胞向肺泡腔的浸润,还抑制了LPS诱导的ALI中的肺水肿。LPS引起的促炎细胞因子如TNFα和IL-6分泌的减少被姜酮醇逆转。LPS诱导的促炎介质iNOS和COX-2的表达被姜酮醇抑制。此外,在LPS诱导的ALI中,姜酮醇抑制了NFκB的激活和Akt的磷酸化。所有这些结果表明,姜酮醇对内毒素诱导的ALI的保护机制是通过抑制Akt-NFκB的激活。

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