Ginkgo biloba extracts protect human retinal Müller glial cells fromt-BHP induced oxidative damage by activating the AMPK-Nrf2-NQO-1 axis

Author:

Li Yue1,Wang Ke2,Zhu Xue2ORCID,Cheng Zhengqi134,Zhu Ling5,Murray Michael1,Zhou Fanfan1ORCID

Affiliation:

1. The University of Sydney, Sydney Pharmacy School, Faculty of Medicine and Health NSW , 2006 , Australia

2. Key Laboratory of Nuclear Medicine, Ministry of Health, Jiangsu Key Laboratory of Molecular Nuclear Medicine, Jiangsu Institute of Nuclear Medicine , Wuxi, Jiangsu Province, 214063 , China

3. Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences , Guangzhou, Guangdong , China

4. Bioland Laboratory (Guangzhou Regenerative Medicine and Health Guangdong Laboratory) , Guangzhou, Guangdong , China

5. The University of Sydney, Save Sight Institute , Sydney, NSW, 2000 , Australia

Abstract

AbstractObjectivesRetinal Müller glial cell loss is almost involved in all retinal diseases, especially diabetic retinopathy (DR). Oxidative stress significantly contributes to the development of Müller glial cell loss. Ginkgo biloba extracts (GBE) have been reported to possess antioxidant property, beneficial in treating human retinal diseases. However, little is known about its role in Müller glial cells. This study investigated the protective effect of GBE (prepared from ginkgo biloba dropping pills) in human Müller glial cells against tert-butyl hydroperoxide (t-BHP)-induced oxidative stress and its underlying molecular mechanism.MethodsMIO-M1 cells were pretreated with or without GBE prior to the exposure to t-BHP-induced oxidative stress. Cell viability, cell death profile and lipid peroxidation were subsequently assessed. Protein expression of the key anti-oxidative signalling factors were investigated.Key findingsWe showed that GBE can effectively protect human MIO-M1 cells from t-BHP-induced oxidative injury by improving cell viability, reducing intracellular ROS accumulation and suppressing lipid peroxidation, which effect is likely mediated through activating AMPK-Nrf2-NQO-1 antioxidant respondent axis.ConclusionsOur study is the first to reveal the great potentials of GBE in protecting human retinal Müller glial cell loss against oxidative stress. GBE might be used to prevent human retinal diseases particularly DR.

Funder

University of Sydney-Wepon post-graduate scholarship, Australia

Wuxi Commission of Health, China

Publisher

Oxford University Press (OUP)

Subject

Pharmaceutical Science,Pharmacology

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