Protective Effect of Polyphenols Purified from Mallotus oblongfolius on Ethanol-Induced Gastric Mucosal Injury by Regulating Nrf2 and MAPKs Pathways
文献类型： 外文期刊
作者： Yu, Shasha 1 ; Duan, Zhouwei 1 ; Li, Peng 5 ; Wang, Shiping 1 ; Guo, Lijun 3 ; Xia, Guanghua 2 ; Xie, Hui 1 ;
作者机构： 1.Hainan Acad Agr Sci, Inst Agroprod Proc & Design, Haikou 571100, Peoples R China
2.Hainan Univ, Coll Food Sci & Technol, Haikou 570228, Peoples R China
3.Hainan Acad Agr Sci, Sanya Inst, Sanya 572000, Peoples R China
4.Huazhong Agr Univ, Coll Food Sci & Technol, Wuhan 430070, Peoples R China
5.Hainan Univ, Coll Feng Xiang, Haikou 570228, Peoples R China
关键词： Mallotus oblongifolius polyphenols (MOP); purification; gastric mucosal injury; oxidative stress; ethanol
期刊名称：ANTIOXIDANTS （ 影响因子：7.675； 五年影响因子：7.886 ）
ISSN：
年卷期： 2022 年 11 卷 12 期
页码：
收录情况： SCI
摘要： Mallotus oblongifolius (MO), which is rich in polyphenols, is a characteristic tea resource with medicinal value. In this study, a total of 45 polyphenolic components of MO, including narirutin, isoquercitrin, rutin and digallic acid, were identified by UPLC-Q-TOF/MS analysis. In addition, the gastroprotective effect of Mallotus oblongifolius polyphenols (MOP) on ethanol-induced gastric mucosal injury in rats was investigated. The rats received anhydrous ethanol after continuous gavage of MOP or lansoprazole for one week. In addition, the macro- and micro-damage induced by ethanol in the gastric tissue was significantly reduced after MOP pretreatment for one week. Further analysis showed that MOP prevented ethanol-induced acute gastric mucosal injury by increasing the expression of antioxidant enzymes (SOD, CAT, GSH-Px) and decreasing the expression of reactive oxygen species (ROS), lipid oxidation product (MDA) and myeloperoxidase (MPO). Meanwhile, MOP inhibited the phosphorylation of p38/ERK/JNK and promoted the activation of the Nrf2 pathway. These results suggested that MOP may be a promising therapeutic target for the prevention of ethanol-induced gastric mucosal injury by improving oxidative stress, inhibiting the p38/ERK/JNK signaling pathways and activating Nrf2 expression.
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