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

<b>Background:</b> 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 <i>Antrodia cinnamomea</i> 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 <i>in vitro</i> and <i>in vivo</i>. <b>Methods:</b> 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. <b>Results:</b> 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 <i>in vivo</i> results, Antcin K protects against CTX-induced skeletal muscle inflammation and injury. <b>Conclusion:</b> Antcin K ameliorated CTX-induced muscle injury and inflammation through PI3K and Akt and upregulated IL-10 <i>in vitro</i>. The CTX-induced injury mouse model was rescued by intraperitoneal injection of Antcin k <i>in vivo</i>. Antcin K shows promise as a prospective candidate for the development of an innovative treatment for muscular injury, with significant implications for sarcopenia.