2. Academic Validation
  3. Antcin K ameliorates cardiotoxin-induced skeletal muscle injury and inflammation via IL-10 regulation

Antcin K ameliorates cardiotoxin-induced skeletal muscle injury and inflammation via IL-10 regulation

  • Int J Biol Sci. 2025 Mar 19;21(6):2493-2507. doi: 10.7150/ijbs.107343.
Ting-Kuo Chang 1 2,  Lin-Chu Huang 3,  Yueh-Hsiung Kuo 4 5,  Chun-Hao Tsai 3 6 7,  Hsien-Te Chen 3 6 8,  Yi-Syuan Wu 3,  Chih-Hsin Tang 5 9 10,  Chen-Ming Su 3
Affiliations

Affiliations

  • 1 Department of Medicine, Mackay Medical College, New Taipei, Taiwan.
  • 2 Division of Spine Surgery, Department of Orthopedic Surgery, MacKay Memorial Hospital, New Taipei, Taiwan.
  • 3 Department of Sports Medicine, China Medical University, Taichung, Taiwan.
  • 4 Department of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, Taiwan.
  • 5 Chinese Medicine Research Center, China Medical University, Taichung, Taiwan.
  • 6 Department of Orthopedic Surgery, China Medical University Hospital, Taichung, Taiwan.
  • 7 School of Medicine, China Medical University, Taichung, Taiwan.
  • 8 Spine Center, China Medical University Hospital, China Medical University, Taichung, Taiwan.
  • 9 Department of Pharmacology, School of Medicine, China Medical University, Taichung, Taiwan.
  • 10 Department of Medical Laboratory Science and Biotechnology, College of Medical and Health Science, Asia University, Taichung, Taiwan.
PMID: 40303299 DOI: 10.7150/ijbs.107343
Abstract

Background: Skeletal muscle, functioning as an endocrine organ, produces a variety of molecules that contribute to the pathophysiology of sarcopenia, leading to muscular injury and inflammation. Antcin K, a bioactive compound derived from Antrodia cinnamomea and used in traditional Chinese medicine for its anti-inflammatory properties, was evaluated in this study with the aim of assessing its effects on resisting the progression of sarcopenia both in vitro and in vivo. Methods: Cardiotoxin (CTX)-induced muscle injury and the treatment of Antcin K in C2C12 cells were both used for RNA Sequencing and ingenuity pathway analysis. We also stably cloned an IL-10 knockdown (IL-10-/+) C2C12 cell line for the effects of Antcin K treatment on CTX-induced muscle injury. CTX-induced muscle injury in a mouse model. Results: Antcin K ameliorated the CTX-induced muscle injury and inflammation in myoblasts and differentiated myocytes. Bioinformatics analysis results demonstrated the ability of Antcin K to modulate inflammation and enhance myogenesis via upregulated IL-10. Antcin K enhances IL-10 production via the PI3K/Akt signaling pathways. For the in vivo results, Antcin K protects against CTX-induced skeletal muscle inflammation and injury. Conclusion: Antcin K ameliorated CTX-induced muscle injury and inflammation through PI3K and Akt and upregulated IL-10 in vitro. The CTX-induced injury mouse model was rescued by intraperitoneal injection of Antcin k in vivo. Antcin K shows promise as a prospective candidate for the development of an innovative treatment for muscular injury, with significant implications for sarcopenia.

Keywords

Antcin K; IL-10; cardiotoxin; inflammation; muscle injury.

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