TY - JOUR A2 - Collino, Massimo AU - Huang, Jinda AU - Peng, Wanwan AU - Zheng, Yijun AU - Hao, Hu AU - Li, Sitao AU - Yao, Yu AU - Ding, Yue AU - Zhang, Junliang AU - Lyu, Juanjuan AU - Zeng, Qiyi PY - 2019 DA - 2019/04/28 TI - Upregulation of UCP2 Expression Protects against LPS-Induced Oxidative Stress and Apoptosis in Cardiomyocytes SP - 2758262 VL - 2019 AB - Uncoupling protein 2 (UCP2) has a cardioprotective role under septic conditions, but the underlying mechanism remains unclear. This study aimed at investigating the effects of UCP2 on the oxidative stress and apoptosis of cardiomyocytes induced by lipopolysaccharide (LPS). First, LPS increased UCP2 expression in cardiomyocytes in a time-dependent manner. LPS increased the production of lactate dehydrogenase (LDH), reactive oxygen species (ROS), and malondialdehyde (MDA) and decreased the level of superoxide dismutase (SOD). However, UCP2 knockdown increased the LPS-induced cardiac injury and oxidative stress. In addition, LPS damaged the mitochondrial ultrastructure and led to the disruption of mitochondrial membrane potential (MMP), as well as the release of mitochondrial cytochrome c. UCP2 knockdown aggravated mitochondrial injury and the release of mitochondrial cytochrome c. LPS increased the protein levels of Bax and cleaved-caspase-3, decreased the protein level of Bcl-2, and upregulated the protein level of mitogen-activated protein kinase. However, upon UCP2 knockdown, the protein levels of Bax and cleaved-caspase-3 increased even further, and the protein level of Bcl-2 was further decreased. The protein level of phosphorylated p38 was also further enhanced. Thus, UCP2 protects against LPS-induced oxidative stress and apoptosis in cardiomyocytes. SN - 1942-0900 UR - https://doi.org/10.1155/2019/2758262 DO - 10.1155/2019/2758262 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -