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芥子碱通过丝裂原活化蛋白激酶(MAPK)和自噬途径抑制活性氧(ROS)诱导的C2C12成肌细胞死亡。

Sinapine suppresses ROS-induced C2C12 myoblast cell death through MAPK and autophagy pathways.

作者信息

Kang Jung Hyun, Kim Dong Hwan, Yoo Jin, Shin Jun Hong, Kim Ju Hyun, Lee Ji Won, Shin Seung Ho

机构信息

Department of Food and Nutrition, Gyeongsang National University, Jinju, 52828 South Korea.

Department of Bio & Medical Bigdata (BK4 Program), Gyeongsang National University, Jinju, 52828 South Korea.

出版信息

Food Sci Biotechnol. 2024 Sep 30;33(15):3629-3637. doi: 10.1007/s10068-024-01718-6. eCollection 2024 Dec.

DOI:10.1007/s10068-024-01718-6
PMID:39493388
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11525351/
Abstract

Oxidative stress in skeletal muscle can lead to muscle atrophy through reactive oxygen species (ROS)-induced damage and cell death. -Butyl hydroperoxide (TBHP), an exogenous ROS generator, induces oxidative stress and cell death in various cells. Sinapine from cruciferous plants possesses beneficial effects, but its role in protecting skeletal muscle cells against ROS-induced cell death remains unclear. This study demonstrates that sinapine pretreatment significantly reduced TBHP-induced cell death and ROS accumulation in a dose-dependent manner. TBHP activated mitogen-activated protein kinase (MAPK) pathways including Akt, p38, and JNK, and triggered autophagy. Sinapine suppressed the phosphorylation of Akt, MEK3/6, p38, MEK4, and JNK, and modulated key autophagy markers. Notably, the co-treatment of MAPK inhibitors attenuated TBHP-induced cell death and LC3B-II accumulation. These findings suggest that sinapine is a promising phytochemical for mitigating oxidative stress-mediated muscle injury, offering potential therapeutic strategies for maintaining skeletal muscle homeostasis and addressing muscle-related pathologies.

摘要

骨骼肌中的氧化应激可通过活性氧(ROS)诱导的损伤和细胞死亡导致肌肉萎缩。叔丁基过氧化氢(TBHP)是一种外源性ROS生成剂,可在各种细胞中诱导氧化应激和细胞死亡。十字花科植物中的芥子碱具有有益作用,但其在保护骨骼肌细胞免受ROS诱导的细胞死亡中的作用仍不清楚。本研究表明,芥子碱预处理以剂量依赖的方式显著降低了TBHP诱导的细胞死亡和ROS积累。TBHP激活了包括Akt、p38和JNK在内的丝裂原活化蛋白激酶(MAPK)途径,并引发自噬。芥子碱抑制了Akt、MEK3/6、p38、MEK4和JNK的磷酸化,并调节关键的自噬标志物。值得注意的是,MAPK抑制剂的联合处理减轻了TBHP诱导的细胞死亡和LC3B-II积累。这些发现表明,芥子碱是一种有前途的植物化学物质,可减轻氧化应激介导的肌肉损伤,为维持骨骼肌稳态和解决肌肉相关病理问题提供潜在的治疗策略。

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