NF-κB介导的蜂毒所致急性肾损伤机制的研究进展  

Advances in the mechanism of NF-κB-mediated acute kidney injury induced by bee venom

作　　者：骆雯鑫 聂小刚 李沙沙 杨翠 张天喜 LUO Wen-xin;NIEXiao-gang;LI Sha-sha;YANG Cui;ZHANG Tian-xi(Department of Emergency,Affiliated Hospital of Zunyi Medical University,Zunyi 563000,Guizhou,CHINA)

机构地区：[1]遵义医科大学附属医院急诊科,贵州遵义563000

出　　处：《海南医学》2025年第5期746-749,共4页Hainan Medical Journal

基　　金：贵州省遵义市联合基金项目(编号:M7yk2022-43)。

摘　　要：蜂蜇伤是一种常见的急性中毒性疾病,由蜂毒中复杂成分(如蜂毒肽和磷脂酶A2)通过直接毒性作用和免疫反应导致多器官损害,尤其是急性肾损伤(AKI)。蜂毒肽通过破坏细胞膜和调控多种细胞信号通路,诱发炎症反应、细胞凋亡和功能紊乱;磷脂酶A2则通过促进炎症介质合成和细胞因子调节放大致炎效应。蜂蜇伤引发的溶血和横纹肌溶解综合征导致代谢紊乱、肾小管阻塞和急性肾小管坏死。此外,蜂毒介导的过敏反应和血管效应进一步减少肾血流量,激活RAAS系统,加重肾缺血损伤。研究表明,NF-κB通路在蜂蜇伤致AKI的形成中发挥重要作用,但其具体机制仍不完全明确。本文从蜂毒成分及其机制出发,探讨NF-κB在蜂蜇伤致AKI中的作用,为临床干预提供理论依据。Bee stings are a common acute toxic condition caused by the complex components of bee venom,such as melittin and phospholipase A2,which induce multi-organ damage through direct toxicity and immune responses,particularly acute kidney injury(AKI).Melittin disrupts cell membranes and regulates multiple signaling pathways,triggering inflammation,apoptosis,and functional disorders.Phospholipase A2 amplifies inflammatory effects by promoting the synthesis of inflammatory mediators and cytokine regulation.Bee stings can cause hemolysis and rhabdomyolysis,leading to metabolic disturbances,tubular obstruction,and acute tubular necrosis.Additionally,venom-induced allergic reactions and vascular effects reduce renal blood flow,activate the renin-angiotensin-aldosterone system(RAAS),and exacerbate renal ischemic injury.Studies suggest that the NF-κB pathway plays a crucial role in AKI induced by bee stings,yet its specific mechanisms remain unclear.This article explores the role of NF-κB in bee sting-induced AKI based on the mechanisms of venom components,providing theoretical insights for clinical intervention.

关 键 词：蜂蜇伤 NF-ΚB 急性肾损伤 肾脏损伤 综述 

分 类 号：R646[医药卫生—外科学]