Protective Effect of Ginkgo biloba Extract (Ginexin(R)) on a Variety of Damage on Cultured RPE.
- Author:
Jong Mo SEO
1
;
Hyeong Gon YU
;
Young Joo KIM
;
Ra Mi KANG
;
Manho KIM
;
Kyu Hyung PARK
;
Hum CHUNG
Author Information
1. Department of Ophthalmology, Seoul National University College of Medicine, Seoul Artificial Eye Center, Seoul National University Hospital Clinical Research Institute, Seoul, Korea. hgonyu@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Ginkgo biloba extract;
Hypoxia;
Oxidative damage;
Retina pigment epithelia;
Ultraviolet damage
- MeSH:
Anoxia;
Apoptosis;
Cell Death;
Flow Cytometry;
Ginkgo biloba*;
Panax;
Retinaldehyde;
Survival Rate;
Trypan Blue;
Vitamin E;
Vitamins
- From:Journal of the Korean Ophthalmological Society
2004;45(6):1017-1023
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: The protective effect of the Ginkgo biloba extract (EGb) on the retinal pigment epithelia (RPE) against ultraviolet, oxidative, and hypoxic damage was investigated. METHODS: Cultured RPE was exposed to ultraviolet B, oxidative damage and hypoxic culture condition after treating with EGb, Vitamin E and red ginseng. Viable RPE after the application of stress was determined by trypan blue assay or MTT assay, and the apoptosis was determined by flow cytometry. Protective effect against the stress by each agent was compared. RESULTS: The group treated with EGb or Vitamin E 1 hour prior to UVB exposure showed a better survival rate than the control group did, and there was no difference in the best survival rate between EGb and Vitamin E. EGb treatment 1 hour before oxidative damage positively affected the survival rate of the RPE. EGb, Vitamin E and red ginseng showed the strongest protective effect against hypoxic damage at the concentration of 0.5 mg/ml, 0.1 mM and 1 mg/ml respectively, with the protective effect of EGb being superior to that of the rest. CONCLUSIONS: These results show that EGb prevents cell death by a variety of damage on RPE, and support the possibility for EGb as a therapeutic agent in the diseases in which RPE damage plays an important role in the pathogenesis.
