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

被引：15
作者：
Tian, Songhao [1 ,2 ]
Zhao, Huiting [3 ]
Guo, Hongru [1 ]
Feng, Wei [1 ]
Jiang, Conglin [1 ]
Jiang, Yusuo [1 ]
机构：
[1] Shanxi Agr Univ, Coll Anim Sci, Taigu 030801, Peoples R China
[2] Shanxi Med Univ, Dept Med Lab, Fenyang Coll, Fenyang 032200, Peoples R China
[3] Shanxi Agr Univ, Coll Life Sci, Taigu 030801, Peoples R China
来源：
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2023年 / 24卷 / 07期
关键词：
PEE; muscle atrophy; aging; D-gal; C2C12; SKELETAL-MUSCLE ATROPHY; GLYCATION END-PRODUCTS; APOPTOSIS; ANTIOXIDANT; EXPRESSION; AUTOPHAGY;
D O I：
10.3390/ijms24076408
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
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页数：13
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