Abstract:

Objective To explore the effects of pretreatment by using the ginkgo biloba extract (GBE) on cell autophagy after rat retina being injured by the ischemiareperfusion and the mechanism on which GBE can protect the retina from ischemia-reperfusion injury. Methods Rats were randomly divided into the following five groups: the normal control group, ischemia-reperfusion model group, and groups intervened by low concentration (1 mg/kg), medium concentration (3 mg/kg), and high concentration (10 mg/kg) of GBE. The retinal ischemia-reperfusion injury model was induced by perfusing the anterior chamber with saline to elevate a hydrostatic pressure of 110 mmHg (1 mmHg=0.133 kPa) for 50 min. The thicknesses of the inner plexiform layer (IPL) and inner nuclear layer (INL) of rat retinas and cell numbers of the ganglion cell layer (GCL) were measured. The apoptosis of retinal cells was detected by the terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphatebiotin nick end labeling (TUNEL). The expression variations of LC3 and Beclin1 which were related to the autophagy were detected by the immunohistochemical staining and Western blotting. Results Compared to the model group, damages of IPL, INL, GCL, and retina of intervention groups (pretreated by GBE of 3 mg/kg and 10 mg/kg) caused by the ischemia-reperfusion injury were significantly decreased (P<0.05); the apoptosis of retinal cells was decreased (P<0.01); the numbers of positive cells of LC3 and Beclin1 were increased (P<0.01); and the expressions of LC3 and Beclin1 were upregulated. Conclusion The mechanism of the protective effects of GBE on the retinal ischemia-reperfusion injury of rats may be related to the upregulation of expressions of Beclin1 and MAP1-LC3 which are related to the autophagy.

Key words: ischemia-reperfusion, retina, autophagy, ginkgo biloba extract