Qiaoju Li1, Zaiwei Zhang2, Hu Li2, Xiaoyu Pan3, Shasha Chen2, Zhiyuan Cui2, Jie Ma2, Zhongxing Zhou2, Bing Xing4. 1. Department of Painless Endoscopy, Jining No.1 People's Hospital, Jining 272011, Shandong, China. 2. Department of Cardiology, Jining No.1 People's Hospital, Jining 272011, Shandong, China. 3. Department of Cardiology, Jining No.1 People's Hospital, Jining 272011, Shandong, China; Jining Medical University, Jining 272067, Shandong, China. 4. Department of Cardiology, Jining No.1 People's Hospital, Jining 272011, Shandong, China. Electronic address: zhzw2001@yeah.net.
Abstract
BACKGROUND: Lycium barbarum polysaccharides (LBPs) are major ingredients of fructus lycii, which have multiple pharmacological activities, such as antioxidant, neuroprotective, and anti-inflammatory activities. This study attempted to reveal the potential of LBPs in hypoxia-injured H9c2 cells and the possible underlying mechanisms. METHODS: H9c2 cells were treated by 300 μg/mL LBPs for 24 h upon hypoxia. Subsequently, the changes in cell viability, migration and apoptosis were evaluated. pre-miR-122 or miR-122 sponge was transfected into H9c2 cells to investigate whether miR-122 was involved in the mechanisms of LBPs' action. Besides, an animal model of myocardial infarction (MI) was established, and the in vivo effects of LBPs were further investigated. RESULTS: LBPs increased cell viability, down-regulated p53, p21 and p16 protein expressions, improved migration, and repressed apoptosis in hypoxia-injured H9c2 cells. miR-122 was highly expressed in response to hypoxia, while was down-regulated by addition of LBPs. The protective actions of LBPs in hypoxia-injured H9c2 cells were attenuated by miR-122 overexpression, while were accelerated by miR-122 suppression. Also, LBPs-induced the activation of MEK/ERK and AMPK signaling pathways were attenuated by miR-122 overexpression, and were accelerated by miR-122 suppression. in vivo investigation revealed that, MI rats administrated with LBPs decreased infarct size and improved cardiac function via down-regulation of miR-122. CONCLUSION: LBPs exhibited in vitro and in vivo cardioprotective activities via down-regulating miR-122. LBPs may have potential for the treatment of acute myocardial infarction (AMI).
BACKGROUND: Lycium barbarum polysaccharides (LBPs) are major ingredients of fructus lycii, which have multiple pharmacological activities, such as antioxidant, neuroprotective, and anti-inflammatory activities. This study attempted to reveal the potential of LBPs in hypoxia-injured H9c2 cells and the possible underlying mechanisms. METHODS: H9c2 cells were treated by 300 μg/mL LBPs for 24 h upon hypoxia. Subsequently, the changes in cell viability, migration and apoptosis were evaluated. pre-miR-122 or miR-122 sponge was transfected into H9c2 cells to investigate whether miR-122 was involved in the mechanisms of LBPs' action. Besides, an animal model of myocardial infarction (MI) was established, and the in vivo effects of LBPs were further investigated. RESULTS: LBPs increased cell viability, down-regulated p53, p21 and p16 protein expressions, improved migration, and repressed apoptosis in hypoxia-injured H9c2 cells. miR-122 was highly expressed in response to hypoxia, while was down-regulated by addition of LBPs. The protective actions of LBPs in hypoxia-injured H9c2 cells were attenuated by miR-122 overexpression, while were accelerated by miR-122 suppression. Also, LBPs-induced the activation of MEK/ERK and AMPK signaling pathways were attenuated by miR-122 overexpression, and were accelerated by miR-122 suppression. in vivo investigation revealed that, MI rats administrated with LBPs decreased infarct size and improved cardiac function via down-regulation of miR-122. CONCLUSION: LBPs exhibited in vitro and in vivo cardioprotective activities via down-regulating miR-122. LBPs may have potential for the treatment of acute myocardial infarction (AMI).