ORIGINAL RESEARCH article
Front. Pharmacol.
Sec. Inflammation Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1524219
This article is part of the Research TopicTargeting Pulmonary Endothelium in Acute Lung Injury and Acute Respiratory Distress SyndromeView all 10 articles
Dexmedetomidine reduces acute lung injury caused by LPS through the SIRT3 signaling pathway in vivo
Provisionally accepted
- Anhui Provincial Children’s Hospital, Hefei, China
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Acute lung injury (ALI) is a clinical syndrome characterized by excessive inflammatory responses. Despite the exploration of various therapeutic approaches, no effective pharmacological treatment is currently available for ALI. In the current study, we investigated the role of SIRT3 in LPS-induced ALI and the potential protective effects of dexmedetomidine (Dex), an agent that activates α2-adrenergic receptors. Histological analysis showed extensive lung damage and increased inflammatory cells in LPS-treated lung samples, with elevated TUNEL+ cells indicating apoptosis (p < 0.05). SIRT3 mRNA and protein expression were significantly downregulated following LPS treatment, both in vivo and in vitro (p < 0.05).DEX administration restored protein SIRT3 levels and reduced inflammation, while the SIRT3 inhibitor 3-TYP negated these benefits (p < 0.05). Additionally, DEX reduced proinflammatory cytokine levels and oxidative stress, effects that were also diminished by 3-TYP (p < 0.05). Our findings suggest that DEX exerts its protective effects against LPS-induced ALI via modulation of the SIRT3/LKB1/AMPK signaling pathway, highlighting the critical role of SIRT3 in inflammatory and oxidative stress responses in ALI.
Keywords: Acute Lung Injury, sirt3, Dexmedetomidine, Inflammation, Oxidative Stress
Received: 07 Nov 2024; Accepted: 12 Jun 2025.
Copyright: © 2025 CHEN, CAI, PENG, XU, CHEN, Xinxin and SUN. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Yingying SUN, Anhui Provincial Children’s Hospital, Hefei, China
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