Effect of Ginkgo biloba extract (EGb50) on mitochondrial function in SH-SY5Y cells after hypoxia/reoxygenation injury.
10.19540/j.cnki.cjcmm.20180613.001
- Author:
Rong YUAN
1
;
Ye-Hao ZHANG
1
;
Bing-Li CHENG
2
;
Wei-Li SHI
1
;
Qi-Qi XIN
1
;
Yan LU
1
;
Wei-Hong CONG
1
Author Information
1. Cardiovascular Laboratory, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
2. West China School of Pharmacy, Sichuan University, Sichuan 610041, China.
- Publication Type:Journal Article
- Keywords:
Ginkgo biloba extract;
SH-SY5Y cell;
energy metabolism;
hypoxia/reoxygenation injury;
mitochondrial function
- MeSH:
Cell Hypoxia;
Humans;
Membrane Potential, Mitochondrial;
Mitochondria;
Plant Extracts;
Reperfusion Injury
- From:
China Journal of Chinese Materia Medica
2018;43(22):4486-4490
- CountryChina
- Language:Chinese
-
Abstract:
Ischemic cerebrovascular disease and cerebral ischemia/reperfusion injury threaten the health of human being. We studied the protective effect of Ginkgo biloba extract 50 (EGb50) on the mitochondrial function in SH-SY5Y cells after hypoxia/reoxygenation (H/R) injury and explored its mechanisms, so as to provide new ideas for studies on the treatment for ischemic cerebrovascular disease. We established the H/R injury model in SH-SY5Y cells after administrating EGb50. Subsequently, the mitochondrial membrane potential and the concentration of intracellular Ca²⁺ were measured by flow cytometer. The levels of optic atrophy1 (Opa1) and dynamin-like protein 1 (Drp1) were evaluated by immunofluorescence and western blot. The results showed that the mitochondrial membrane potential was decreased and the level of intracellular Ca²⁺ was increased after H/R injury. Moreover, the expression of mitochondrial fusion protein Opa1 was decreased, while the expression of mitochondrial fission protein Drp1 was increased. However, EGb50 significantly increased the mitochondrial membrane potential and suppressed the level of intracellular Ca²⁺. In addition, EGb50 increased the expression of Opa1 and decreased the expression of Drp1. The results demonstrated that EGb50 has a neuroprotective effect on SH-SY5Y cells after H/R injury, and could improve the energy metabolism and mitochondrial function. The underlying mechanisms may be associated with the regulation of mitochondrial fusion and fission, which provided data support for the treatment of ischemic cerebrovascular disease with EGb50.
