Activation of the AMPK/Nrf2 pathway ameliorates LPS-induced acute lung injury by inhibiting oxidative stress and reducing inflammation.

IF 1.5 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Journal of Cardiothoracic Surgery Pub Date : 2024-10-01 DOI:10.1186/s13019-024-03020-2
Haoxuan Li, Yiting Nie, Hongyu Hui, Xinxin Jiang, Yuanyuan Xie, Cong Fu
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Abstract

Background: Numerous diseases-related acute lung injury (ALI) contributed to high mortality. Currently, the therapeutic effect of ALI was still poor. The detailed mechanism of ALI remained elusive and this study aimed to elucidate the mechanism of ALI.

Method: This study was performed to expose the molecular mechanisms of AMPK/Nrf2 pathway regulating oxidative stress in LPS-induced AMI mice. The mouse ALI model was established via intraperitoneal injection of LPS, then the lung tissue and blood samples were obtained, followed by injection with Dimethyl fumarate (DMF). Finally, Western blot, HE staining, injury score, lung wet/dry ratio, reactive oxygen species (ROS) and ELISA were used to elucidate the mechanism of AMPK/Nrf2 pathway in LPS -induced acute lung injury by mediating oxidative stress.

Results: The lung tissue injury score was evaluated, showing higher scores in the model group compared to the AMPK activator and control groups. DCFH-DA indicated that LPS increased ROS production, while AMPK activator DMF reduced it, with the model group exhibiting higher ROS levels than the control and AMPK activator groups. The lung wet/dry ratio was also higher in the model group. Western blot analysis revealed LPS reduced AMPK and Nrf2 protein levels, but DMF reversed this effect. ELISA results showed elevated IL-6 and IL-1β levels in the model group compared to the AMPK activator and control groups.

Conclusion: CONCLUSION: Activating the AMPK/Nrf2 pathway can improve LPS-induced acute lung injury by down-regulation of the oxidative stress and corresponding inflammatory factor level.

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通过抑制氧化应激和减少炎症,激活 AMPK/Nrf2 通路可改善 LPS 诱导的急性肺损伤。
背景:与多种疾病相关的急性肺损伤(ALI)导致了很高的死亡率。目前,ALI 的治疗效果仍然不佳。ALI的详细机制仍然难以捉摸,本研究旨在阐明ALI的机制:本研究旨在揭示 AMPK/Nrf2 通路调节 LPS 诱导的 AMI 小鼠氧化应激的分子机制。通过腹腔注射 LPS 建立小鼠 ALI 模型,获取肺组织和血液样本,然后注射富马酸二甲酯(DMF)。最后,利用 Western 印迹、HE 染色、损伤评分、肺干湿比、活性氧(ROS)和 ELISA 等方法阐明了 AMPK/Nrf2 通路通过介导氧化应激在 LPS 诱导的急性肺损伤中的作用机制:结果:对肺组织损伤评分进行了评估,结果显示模型组的评分高于 AMPK 激活剂组和对照组。DCFH-DA 表明 LPS 增加了 ROS 的产生,而 AMPK 激活剂 DMF 则减少了 ROS 的产生,模型组的 ROS 水平高于对照组和 AMPK 激活剂组。模型组的肺干湿比也更高。Western 印迹分析显示,LPS 降低了 AMPK 和 Nrf2 蛋白水平,但 DMF 逆转了这一效应。ELISA结果显示,与AMPK激活剂组和对照组相比,模型组的IL-6和IL-1β水平升高:结论:激活 AMPK/Nrf2 通路可通过下调氧化应激和相应的炎症因子水平来改善 LPS 诱导的急性肺损伤。
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来源期刊
Journal of Cardiothoracic Surgery
Journal of Cardiothoracic Surgery 医学-心血管系统
CiteScore
2.50
自引率
6.20%
发文量
286
审稿时长
4-8 weeks
期刊介绍: Journal of Cardiothoracic Surgery is an open access journal that encompasses all aspects of research in the field of Cardiology, and Cardiothoracic and Vascular Surgery. The journal publishes original scientific research documenting clinical and experimental advances in cardiac, vascular and thoracic surgery, and related fields. Topics of interest include surgical techniques, survival rates, surgical complications and their outcomes; along with basic sciences, pediatric conditions, transplantations and clinical trials. Journal of Cardiothoracic Surgery is of interest to cardiothoracic and vascular surgeons, cardiothoracic anaesthesiologists, cardiologists, chest physicians, and allied health professionals.
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