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Article Publish Status: FREE
Abstract Title:

Hyperoside Protected Against Oxidative Stress-Induced Liver Injurythe PHLPP2-AKT-GSK-3β Signaling Pathwayand.

Abstract Source:

Front Pharmacol. 2020 ;11:1065. Epub 2020 Jul 17. PMID: 32765271

Abstract Author(s):

Haiyan Xing, Ruoqiu Fu, Caiyi Cheng, Yongqing Cai, Xianfeng Wang, Dongmei Deng, Xiaoyuan Gong, Jianhong Chen

Article Affiliation:

Haiyan Xing

Abstract:

Hyperoside, isolated fromL., seeds ofLam., orL., originally showed to possess an antifungal and antibacterial activity, while recently showed the protective effects against oxidative stress-induced liver injury. This study investigated such a protective effect of hyperoside and the underlying molecular mechanismsand in carbon tetrachloride (CCl4)-injured rat livers. The data showed that hyperoside was able to prevent the oxidative stress-induced liver morphological changes and CCl4-induced rat liver injury. Hyperoside reversed the decrease of superoxidase dismutase (SOD) level and the increase of malondialdehyde (MDA) level. Moreover, hyperoside regulated the pleckstrin homology (PH) domain leucine-rich repeat protein phosphatase 2 (PHLPP2)-protein kinase B (AKT)-glycogen synthase kinase 3β (GSK-3β) signaling pathway in tert-butylhydroquinone (t-BHP)-treated liver cells, e.g., Hyperoside reduced PHLPP2 expression to activate AKT phosphorylation, induce GSK-3β phosphorylation, and then increased nuclear factor erythroid-2-related factor 2 (Nrf2) nuclear translocation, reduced nuclear translocation of phosphorylated Fyn, and promoted heme oxygenase-1 (HO-1) expressionand. In contrast, siRNA-mediated knockdown of PHLPP2 expression enhanced hyperoside-mediated activation of the AKT-GSK-3β kinase pathway in liver cells. In conclusion, the present study demonstrated that hyperoside could protect against oxidative stress-induced liver injury by regulating the PHLPP2-AKT-GSK-3β signaling pathwayand.

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