Propolis Ethanolic Extract Attenuates D-gal-induced C2C12 Cell Injury by Modulating Nrf2/HO-1 and p38/p53 Signaling Pathways

Previous study has shown that propolis ethanolic extract (PEE) has a protective effect on aging skeletal muscle atrophy. However, the exact molecular mechanism remains unclear. This study aimed to investigate the effect of PEE on D-galactose (D-gal)-induced damage in mouse C2C12 cells. The results revealed that PEE increased the viability of senescent C2C12 cells, decreased the number of senescence-associated beta-galactosidase (SA-beta-Gal)-positive cells and promoted the differentiation of C2C12 cells. PEE resisted oxidative stress caused by D-gal by activating the Nrf2/HO-1 signaling pathway and maintained the differentiation ability of C2C12 cells. PEE inhibited apoptosis by suppressing p38 phosphorylation and reducing p53 expression. In summary, our findings reveal the molecular mechanism by which PEE protects D-gal-induced C2C12 cells, providing a theoretical basis for the development of PEE for the alleviation of muscle atrophy.

Automated summary

This study investigated the effect of propolis ethanolic extract (PEE) on D-galactose-induced damage in mouse C2C12 cells. The results showed that PEE increased cell viability, decreased senescence-associated beta-galactosidase-positive cells, and promoted cell differentiation. PEE protected cells from oxidative stress by activating the Nrf2/HO-1 signaling pathway, and inhibited apoptosis by suppressing p38 phosphorylation and reducing p53 expression. These findings provide a theoretical basis for the use of PEE in alleviating muscle atrophy.