ω-3 PUFAs Alleviate GJ-Cx43 Uncoupling Induced by Long-Term Isoflurane Exposure by Activating the Wnt/β-catenin Signaling Pathway in Astrocytes.

IF 3.3 3区生物学 Q3 CELL BIOLOGY

Cell Biology International Pub Date : 2025-05-13 DOI:10.1002/cbin.70028

Zimo Wang, Rui Dong, Yuqiang Han, Liangyu Peng, Shuai Liu, Zhengliang Ma, Tianjiao Xia, Xiaoping Gu

引用次数: 0

Abstract

Isoflurane, a widely used anesthetic, has raised concerns due to its potential neurotoxic effects, including oxidative stress and astrocytic gap junction (GJ) dysfunction. This study investigates whether ω-3 polyunsaturated fatty acids (PUFAs), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), can mitigate these effects by activating the Wnt/β-catenin signaling pathway. Using primary astrocytes, we found that long-term isoflurane exposure uncoupled GJ-Cx43, increased reactive oxygen species (ROS), and inhibited Wnt/β-catenin signaling. ω-3 PUFA treatment restored GJ-Cx43 coupling, reduced ROS levels, and partially reactivated the Wnt/β-catenin pathway. These findings suggest that ω-3 PUFAs protect against isoflurane-induced neurotoxicity by enhancing GJ-Cx43 coupling and reducing oxidative stress, offering a potential therapeutic strategy for perioperative neurocognitive disorders."

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ω-3 PUFAs通过激活星形胶质细胞Wnt/β-catenin信号通路缓解长期异氟醚暴露诱导的GJ-Cx43解偶联

异氟醚是一种广泛使用的麻醉剂，由于其潜在的神经毒性作用，包括氧化应激和星形细胞间隙连接（GJ）功能障碍，引起了人们的关注。本研究探讨ω-3多不饱和脂肪酸（PUFAs），特别是二十二碳六烯酸（DHA）和二十碳五烯酸（EPA）是否可以通过激活Wnt/β-catenin信号通路来减轻这些影响。通过对原代星形胶质细胞的研究，我们发现长期暴露于异氟醚可以解耦GJ-Cx43，增加活性氧（ROS），抑制Wnt/β-catenin信号传导。ω-3 PUFA处理恢复GJ-Cx43偶联，降低ROS水平，部分重新激活Wnt/β-catenin通路。这些发现表明ω-3 PUFAs通过增强GJ-Cx43偶联和减少氧化应激来保护异氟醚诱导的神经毒性，为围手术期神经认知障碍提供了一种潜在的治疗策略。”

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Cell Biology International 生物-细胞生物学

CiteScore

7.60

自引率

0.00%

发文量

208

审稿时长

1 months

期刊介绍： Each month, the journal publishes easy-to-assimilate, up-to-the minute reports of experimental findings by researchers using a wide range of the latest techniques. Promoting the aims of cell biologists worldwide, papers reporting on structure and function - especially where they relate to the physiology of the whole cell - are strongly encouraged. Molecular biology is welcome, as long as articles report findings that are seen in the wider context of cell biology. In covering all areas of the cell, the journal is both appealing and accessible to a broad audience. Authors whose papers do not appeal to cell biologists in general because their topic is too specialized (e.g. infectious microbes, protozoology) are recommended to send them to more relevant journals. Papers reporting whole animal studies or work more suited to a medical journal, e.g. histopathological studies or clinical immunology, are unlikely to be accepted, unless they are fully focused on some important cellular aspect. These last remarks extend particularly to papers on cancer. Unless firmly based on some deeper cellular or molecular biological principle, papers that are highly specialized in this field, with limited appeal to cell biologists at large, should be directed towards journals devoted to cancer, there being very many from which to choose.