首页|Bax/Bcl-2介导胡蜂蛰伤致急性肾损伤机制的研究进展

Bax/Bcl-2介导胡蜂蛰伤致急性肾损伤机制的研究进展

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重度胡蜂蜇伤常引发急性肾损伤(AKI),且其发生与疾病严重程度、重症监护时间以及不良预后密切相关。这一病理过程的机制通常被认为与蜂毒的毒性作用及其诱导的炎症和免疫反应有关。蜂毒能够直接作用于肾小管,导致肾小管上皮细胞凋亡,同时通过介导免疫炎症反应进一步加重肾功能障碍。然而,具体的分子作用机制尚未完全阐明。Bax与Bcl-2的平衡在维持细胞稳态和功能方面起着关键作用。既往研究表明,Bax/Bcl-2的过度表达可通过激活肿瘤坏死因子α(TNF-α)通路,诱导内皮细胞凋亡及炎症反应,从而引起AKI的发生。然而,关于Bax/Bcl-2平衡在胡蜂毒引发的AKI中的研究相对较少。本文将从Bax/Bcl-2介导细胞凋亡的作用机制出发,结合最新研究进展,综述胡蜂蜇伤后的相关机制,并探讨Bax/Bcl-2在AKI治疗中的潜在应用前景。
Research progress on the mechanism of acute renal injury induced by wasp stings injury mediated by Bax/Bcl-2
Severe wasp stings often lead to acute kidney injury(AKI),and its occurrence is closely associated with disease severity,intensive care unit(ICU)stay,and poor prognosis.The mechanism of this pathological process is generally believed to be related to the toxic effects of wasp venom and the inflammatory and immune responses it induc-es.Wasp venom can directly affect renal tubules,leading to apoptosis of renal tubular epithelial cells,while also exacer-bating renal dysfunction by mediating immune-inflammatory responses.However,the specific molecular mechanisms are not yet fully elucidated.The balance between Bax and Bcl-2 plays a key role in maintaining cellular homeostasis and function.Previous studies have shown that the overexpression of Bax/Bcl-2 can induce endothelial cell apoptosis and in-flammation through the activation of the TNF-α pathway,contributing to the development of AKI.However,research on the role of Bax/Bcl-2 balance in wasp venom-induced AKI is relatively scarce.This paper will review the relevant mech-anisms of wasp stings,focusing on the apoptotic mechanisms mediated by Bax/Bcl-2,and discuss the potential applica-tion prospects of Bax/Bcl-2 in the treatment of AKI based on the latest research.

Bax/Bcl-2Wasp stingsAcute renal injuryApoptosisPathogenesis

聂小刚、骆雯鑫、陈荣辉、刘杰、张天喜

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遵义医科大学附属医院急诊科,贵州 遵义 563003

Bax/Bcl-2 胡蜂蜇伤 急性肾损伤 细胞凋亡 发病机制

2025

海南医学
海南省医学会

海南医学

影响因子:1.158
ISSN:1003-6350
年,卷(期):2025.36(1)