Oyster polysaccharide alleviates TNF-α-induced muscle atrophy via regulation of the calcium signalling pathway in C2C12 myoblasts

Bingna Cai; Ailing Duan; Hua Chen; Si Li; Xiangtan Zhao; Peng Wan; Deke Chen; Xin Chen; Jianyu Pan

doi:10.1016/j.ijbiomac.2025.145608

Oyster polysaccharide alleviates TNF-α-induced muscle atrophy via regulation of the calcium signalling pathway in C2C12 myoblasts

Int J Biol Macromol. 2025 Jun 26:145608. doi: 10.1016/j.ijbiomac.2025.145608. Online ahead of print.

Authors

Bingna Cai¹, Ailing Duan¹, Hua Chen¹, Si Li¹, Xiangtan Zhao¹, Peng Wan¹, Deke Chen¹, Xin Chen², Jianyu Pan³

Affiliations

¹ Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Key Laboratory of Marine Materia Medica, South China Sea Institute of Oceanology, Chinese Academy of Sciences, 164 West Xingang Road, Guangzhou 510301, Guangdong, China.
² International School, Foshan University, Foshan 528225, Guangdong, China.
³ Key Laboratory of Tropical Marine Bio-resources and Ecology, Guangdong Key Laboratory of Marine Materia Medica, South China Sea Institute of Oceanology, Chinese Academy of Sciences, 164 West Xingang Road, Guangzhou 510301, Guangdong, China.. Electronic address: jypan@scsio.ac.cn.

PMID: 40581020
DOI: 10.1016/j.ijbiomac.2025.145608

Abstract

This study aimed to elucidate how Crassostrea hongkongensis polysaccharide (CHP) alleviates TNF-α-induced atrophy in C2C12 myotubes. CHP enhances MyHC expression while suppressing the muscle atrophy markers MuRF1 and MaFbx. Additionally, CHP significantly enhanced mitochondria biogenesis and ATP production. This effect may be attributed to CHP induced activation of glucagon and glycolysis/gluconeogenesis signalling pathways, as well as its modulation of insulin resistance. Transcriptomic analyses demonstrated that CHP attenuated the TNF-α mediated inhibition of C2C12 myoblast differentiation and multinucleated myotubes formation, potentially through modulation of calcium signalling pathways. Molecular docking, molecular dynamics, and quantum chemical assessments suggest that the branched structure of CHP molecules promotes flexible electron distribution. This stabilizes the binding of CHP to sarco/endoplasmic reticulum calcium ATPase (SERCA), which is crucial for calcium reuptake. Consequently, CHP upregulates energy metabolism pathways to improve mitochondrial function, increases the SERCA expression to promote calcium reuptake, thereby alleviating muscle waste.

Keywords: C2C12 myoblast; Muscle atrophy; Oyster polysaccharide.