Toxicon : official journal of the International Society on Toxinology · 2026
Cyclosporine A protects against wasp venom-induced rhabdomyolysis in rats by inhibiting the CypD-mPTP pathway.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Shasha, Deng Fangfang, Yang Cui, Liu Shengshan, Zhou Jie, Guo Fujian, Yu Anyong, Zhang Tianxi
Аннотация
OBJECTIVE: Wasp venom-induced rhabdomyolysis (RM) is a life-threatening syndrome characterized by skeletal muscle damage and systemic complications. The core mechanism is closely associated with mitochondrial-mediated energy metabolism disturbances. This study aims to investigate the role of the mitochondrial-mediated Cyclophilin D (CypD)-mitochondrial permeability transition pore (mPTP) pathway in wasp venom-induced RM and the protective mechanism of cyclosporine A (CsA).
METHODS: Rats were randomly assigned to five groups according to a random number table: control group, normal saline (NS) group, CsA monotherapy group, venom control group (V) group, and V + CsA intervention group.
RESULTS: Compared to the control group, the V group exhibited significantly elevated serum levels of CK, AST, ALT, and Cr (P < 0.01). Additionally, levels of pro-inflammatory cytokines (IL-2, IFN-γ, TGF-β) were notably increased (P < 0.01). Histological examinations of skeletal muscle tissue revealed significant myofiber disruption, myocyte lysis and necrosis, mitochondrial structural damage, and signs of apoptosis. Furthermore, the total protein expressions of cytochrome c (CytC), caspase-3 (Caspase-3), and CypD were all significantly upregulated (P < 0.01). Treatment with CsA significantly ameliorated these injuries.
CONCLUSION: This study successfully established a rat model of wasp venom-induced rhabdomyolysis. The abnormal opening of the CypD-mediated mPTP is one of the potential mechanisms underlying wasp venom-induced RM. CsA mitigates RM by inhibiting the CypD-mPTP pathway, providing a new therapeutic target for muscle injury induced by wasp venom.
METHODS: Rats were randomly assigned to five groups according to a random number table: control group, normal saline (NS) group, CsA monotherapy group, venom control group (V) group, and V + CsA intervention group.
RESULTS: Compared to the control group, the V group exhibited significantly elevated serum levels of CK, AST, ALT, and Cr (P < 0.01). Additionally, levels of pro-inflammatory cytokines (IL-2, IFN-γ, TGF-β) were notably increased (P < 0.01). Histological examinations of skeletal muscle tissue revealed significant myofiber disruption, myocyte lysis and necrosis, mitochondrial structural damage, and signs of apoptosis. Furthermore, the total protein expressions of cytochrome c (CytC), caspase-3 (Caspase-3), and CypD were all significantly upregulated (P < 0.01). Treatment with CsA significantly ameliorated these injuries.
CONCLUSION: This study successfully established a rat model of wasp venom-induced rhabdomyolysis. The abnormal opening of the CypD-mediated mPTP is one of the potential mechanisms underlying wasp venom-induced RM. CsA mitigates RM by inhibiting the CypD-mPTP pathway, providing a new therapeutic target for muscle injury induced by wasp venom.