Adiponectin modulates oxidative stress-induced mitophagy and protects C2C12 myoblasts against apoptosis

Scientific Reports

卷:7

Long Jia¹  Mingkun Ma¹  Yinghui Ren¹  Dongmei Zhou¹  Yurong Da¹  Qi Zhang¹  Hongkun Liu¹  Huipeng Yang¹  Lijuan Zhang¹  Zhenyi Xue¹  Yan Li¹  Zimu Zhang¹  Rongxin Zhang¹  Shuqin Mu²  Jun Yan² 

[1] Department of Immunology, Research Center of Basic Medical Sciences, Key Laboratory of Immune Microenvironment and Diseases of Educational Ministry of China, Tianjin Medical University;

[2] Tianjin Institute of Animal husbandry and veterinary, Tianjin Academy of Agricultural Science;

关键词: ;   

DOI  :  10.1038/s41598-017-03319-2

来源: DOAJ

【 摘 要 】

Abstract Adiponectin (APN), also known as apM1, Acrp30, GBP28 and adipoQ, is a circulating hormone that is predominantly produced by adipose tissue. Many pharmacological studies have demonstrated that this protein possesses potent anti-diabetic, anti-atherogenic and anti-inflammatory properties. Although several studies have demonstrated the antioxidative activity of this protein, the regulatory mechanisms have not yet been defined in skeletal muscles. The aim of the present study was to examine the cytoprotective effects of APN against damage induced by oxidative stress in mouse-derived C2C12 myoblasts. APN attenuated H2O2-induced growth inhibition and exhibited scavenging activity against intracellular reactive oxygen species that were induced by H2O2. Furthermore, treating C2C12 cells with APN significantly induced heme oxygenase-1 (HO-1) and nuclear factor-erythroid 2 related factor 2 (Nrf2). APN also suppressed H2O2-induced mitophagy and partially inhibited the colocalization of mitochondria with autophagosomes/lysosomes, correlating with the expression of Pink1 and Parkin and mtDNA. Moreover, APN protected C2C12 myoblasts against oxidative stress-induced apoptosis. Furthermore, APN significantly reduced the mRNA and protein expression levels of Bax. These data suggest that APN has a moderate regulatory role in oxidative stress-induced mitophagy and suppresses apoptosis. These findings demonstrate the antioxidant potential of APN in oxidative stress-associated skeletal muscle diseases.

【 授权许可】

Unknown