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<p>Envenomation by <i>Trimeresurus stejnegeri</i> induces severe skeletal muscle injury, and while Snakebite Capsules show therapeutic efficacy, their underlying mechanism remains unclear. This study explores the role of ferroptosis in this pathology and the protective effect of Snakebite Capsules. <i>T. stejnegeri</i> envenomation causes significant hemotoxicity and local tissue damage. Despite the clinical efficacy of Snakebite Capsules, their protective mechanism remains incompletely understood, particularly in relation to ferroptosis. Using a rabbit model of <i>T. stejnegeri</i> envenomation, we explored the role of ferroptosis and evaluated the therapeutic potential of Snakebite Capsules. Rescue experiments included the use of ferroptosis modulators Ferrostatin-1 and Erastin. Our results demonstrated that the venom activates ferroptosis, as evidenced by skeletal muscle myofibril dissolution, increased reactive oxygen species (ROS), decreased glutathione (GSH) levels, accumulation of malondialdehyde (MDA) and lipid peroxides (LPO), and dysregulation of key ferroptosis-related proteins. Treatment with Snakebite Capsules significantly attenuated skeletal muscle injury, restored redox homeostasis, and normalized the expression of ferroptosis-associated proteins. These findings indicate that ferroptosis activation is a key mechanism in <i>T. stejnegeri</i> venom-induced muscle damage. We conclude that Snakebite Capsules confer protection at least partially through modulation of the ferroptosis pathway, identifying ferroptosis as a critical target in treating such envenomations.</p>

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Snakebite capsules attenuate Trimeresurus stejnegeri venom-induced skeletal muscle injury by inhibiting the ferroptosis pathway

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月31日

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  • Dan Shao,
  • Jianxin Zheng,
  • Jianzhen Zheng,
  • Meiying Chen,
  • Shaohua He,
  • Shuling Huang,
  • Dan Wen,
  • Hui Wu

摘要

Envenomation by Trimeresurus stejnegeri induces severe skeletal muscle injury, and while Snakebite Capsules show therapeutic efficacy, their underlying mechanism remains unclear. This study explores the role of ferroptosis in this pathology and the protective effect of Snakebite Capsules. T. stejnegeri envenomation causes significant hemotoxicity and local tissue damage. Despite the clinical efficacy of Snakebite Capsules, their protective mechanism remains incompletely understood, particularly in relation to ferroptosis. Using a rabbit model of T. stejnegeri envenomation, we explored the role of ferroptosis and evaluated the therapeutic potential of Snakebite Capsules. Rescue experiments included the use of ferroptosis modulators Ferrostatin-1 and Erastin. Our results demonstrated that the venom activates ferroptosis, as evidenced by skeletal muscle myofibril dissolution, increased reactive oxygen species (ROS), decreased glutathione (GSH) levels, accumulation of malondialdehyde (MDA) and lipid peroxides (LPO), and dysregulation of key ferroptosis-related proteins. Treatment with Snakebite Capsules significantly attenuated skeletal muscle injury, restored redox homeostasis, and normalized the expression of ferroptosis-associated proteins. These findings indicate that ferroptosis activation is a key mechanism in T. stejnegeri venom-induced muscle damage. We conclude that Snakebite Capsules confer protection at least partially through modulation of the ferroptosis pathway, identifying ferroptosis as a critical target in treating such envenomations.