Effect of ginsenoside Rb1 on oxidative damage of human retinal pigment epithelial cells induced by 4-hydroxynonenal

Journals

Online: 17 October 2022; Volume 1, Issue 1, No.4 PDF DOWNLOAD

Title：
Effect of ginsenoside Rb1 on oxidative damage of human retinal pigment epithelial cells induced by 4-hydroxynonenal
Author：
Yue-ying Yu, Lian-ji Tian, Tian-tian Zhao, Mei-hong Jin, Ren-zhe Cui, Jun Cui
Author Affiliation：
Department of Ophthalmology, Affiliated Hospital of Yanbian University, Yanji, China

Abstract

Objective: To study the protective effect of ginsenoside Rb1 on oxidative damage of human retinal pigment epithelial cells (ARPE-19) induced by 4-hydroxynonenal (4-HNE) and its mechanism. Methods: CCK-8 method was used for detecting the concentration of ginsenoside Rb1 and 4-HNE. ARPE-19 cells were randomly divided into Control Group, Rb1 Treatment Group, 4-HNE Group and 4-HNE+RE1 Treatment Group. The morphological structure of cells in each group was observed by light microscope, and the content of reactive oxygen species (ROS) in cells was detected by fluorescence microscope. Western blot was used for detecting the expression level of apoptosis related factors B cell lymphoma (Bcl) - 2 and Bax protein. Results: CCK-8 showed that the concentration of ginsenoside Rb1 was 100 μmol/L when ARPE-19 cells have the highest proliferation rate and better protection, so 100 μmol/L ginsenoside Rb1 for subsequent experiments. Compared with 4-HNE Group, 50.0μmol/L and 100.0 μmol/L. The cell activity in ginsenoside Rb1 Group was significantly increased (P<0.05). Compared with the Control Group, the ROS content in cells of 4-HNE Group increased significantly (P<0.05), the expression of Bax protein increased, and the expression of Bcl-2 protein decreased. Compared with 4-HNE Group, 4-HNE+Rb1 Treatment Group significantly reduced the intracellular ROS content (P<0.05), Bax protein expression decreased, and Bcl-2 protein expression increased. Conclusion: Ginsenoside Rb1 can improve the oxidative damage of RPE cells induced by 4-HNE, and the mechanism may be related to the reduction of apoptosis by ginsenoside Rb1.

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