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Dexmedetomidine attenuates LPS-induced acute lung injury via activation of mitochondrial autophagy

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Editor's note
Mitochondrial quality control through selective autophagy (mitophagy) may be a tractable target in sepsis-induced lung injury, as this rat study shows a sedative drug reduces inflammation and organ damage by clearing damaged mitochondria. The finding is mechanistically plausible but preliminary; translation to critically ill patients requires human validation. Intensivists managing acute respiratory distress syndrome and mitochondrial disease researchers should follow developments here.

Source: openalex · Origin: CN · Huaixin Xing, Yan Ma, Xiangzhen Min, Yingui Sun, Guanrong Li · European journal of medical research · 2026-05-26

URL: https://doi.org/10.1186/s40001-026-04591-7

AI rationale (4/5, tier: preliminary): Directly addresses mitophagy (PINK1/Parkin pathway) mechanism in disease model, but animal study limits evidence tier.

This study aimed to examine the impact of Dex on ALI and clarify the mechanisms, particularly regarding mitophagy. The assignment of male Sprague–Dawley rats was random, with rats going to the control, LPS, and LPS + Dex groups. In vitro, the NR8383 rat alveolar macrophage cell line was treated with LPS and Dex. Techniques such as ELISA, lung wet-to-dry ratio measurement, histologic examination, TUNEL assay, Western blot analysis, CCK-8, real-time quantitative PCR, and mitochondrial membrane potential assessment were used to evaluate inflammatory responses, oxidative stress, mitophagy-related protein and gene expression, and cell viability. Dex treatment significantly attenuated LPS-induced lung histopathological damage and reduced the lung wet-to-dry ratio in rats. It decreased serum and supernatant levels of IL-6 and TNF-α, and lowered intracellular ROS in both lung tissue and NR8383 alveolar macrophages. Mechanistically, Dex significantly upregulated the expression of PINK1, Parkin, and LC3B at both the protein and mRNA levels, and restored mitochondrial membrane potential (MMP) in LPS-injured cells. Pharmacological inhibition of mitophagy with 3-MA reversed these protective effects, whereas the autophagy agonist Hexadecadrol further enhanced them. These findings suggest that Dex alleviates ALI by activating PINK1/Parkin-mediated mitophagy and suppressing the associated inflammatory and oxidative stress responses. Dex attenuates LPS-induced ALI by activating PINK1/Parkin-mediated mitophagy, restoring mitochondrial membrane potential, and reducing inflammation and oxidative stress. These findings suggest that targeting mitophagy may represent a promising therapeutic strategy for ALI.

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Published 2026-05-28 · Last kit-update 2026-05-28