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

  • Int J Mol Sci. 2023 Mar 29;24(7):6408. doi: 10.3390/ijms24076408.
Songhao Tian  1  2 ,  Huiting Zhao  3 ,  Hongru Guo  1 ,  Wei Feng  1 ,  Conglin Jiang  1 ,  Yusuo Jiang  1
Affiliations
  • 1. College of Animal Science, Shanxi Agricultural University, Taigu 030801, China.
  • 2. Department of Medical Laboratory, Fenyang College of Shanxi Medical University, Fenyang 032200, China.
  • 3. College of Life Sciences, Shanxi Agricultural University, Taigu 030801, China.
PMID: 37047379 DOI: 10.3390/ijms24076408
Abstract

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 β-galactosidase (SA-β-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.

Keywords
C2C12; D-gal; PEE; aging; muscle atrophy.
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