Authors
Tonghan Li, Xuan Zhao, Zhikai Xu, Fan Yang, Zhanfei Li, Xiangjun Bai, Hao Zhu, Hong Zhao, Yukun Liu, Yuchang Wang
Lab
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Journal
Shock
Abstract
Plain Language SummaryThis study tested whether selenomethionine (Se-Met) can protect against sepsis-induced skeletal muscle atrophy and explored how it works. In a mouse cecal ligation and puncture model, Se-Met improved survival, body weight, muscle strength, and muscle fiber size. Se-Met reduced expression of Atrogin-1 and MuRF1, key proteins driving muscle protein degradation. In septic mice, Se-Met inhibited the NLRP3/Caspase-1/GSDMD pyroptosis pathway and reduced inflammatory cytokines such as IL-18 and IL-1β in skeletal muscle. In lipopolysaccharide-stimulated C2C12 myoblasts, Se-Met lowered reactive oxygen species and malondialdehyde, increased antioxidant enzymes (superoxide dismutase and glutathione peroxidase), and suppressed pyroptosis by inhibiting the ROS/NLRP3/Caspase-1/GSDMD pathway and inflammatory cytokines including IL-6 and IL-18. These findings support Se-Met as a potential therapy for sepsis-related and other oxidative stress-related muscle injury.
Keywords/Topics
septic mice; effective therapeutic strategies; selenomethionine; se-met; sepsis-induced skeletal muscle atrophy; improved survival; body weight; muscle strength; muscle fiber size; se-met reduced expression
Source :
Congrès & Meetings 2026 