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| Study on the protective effect of ginsenoside Rg1 on optic nerve injury in rats |
| HU Chuxuan LI Suihua ZHANG Xia MEI Qinghua |
| Department of Pharmacy, Guangdong Second People's Hospital, Guangdong Province, Guangzhou 510317, China |
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Abstract Objective To observe the protective effect of ginsenoside Rg1 on optic nerve injury in rats and its protective mechanism. Methods Wistar rats were randomly divided into control group, model group and treatment group, with 30 rats in each group. Rats in the control group were injected intraperitoneally with saline without modeling. Rats in the model group were intraperitoneally injected with saline. Rats in the treatment group were intraperitoneally injected with ginsenoside Rg1 (50 mg/kg) for 7 d. The model of optic nerve injury was established by occlusion of the optic nerve. After 5 days of modeling, fluorescein-labeled retinal ganglion cells (RGCs) were injected into the right superior colliculus on the right side of the rats. Flash visual evoked potentials were detected before the rats were sacrificed. RGCs density, apoptosis of RGCs, P1 wave of evoked potential, optic nerve cholesterol content, silent information regulator 1 (SIRT1) protein and HMG-CoA reductase (HMGCR) expression were detected after the rats were sacrificed. Results At 7, 14, 21 days after sacrifice, the visual evoked potentials and the number of retinal apoptotic cells in the control group did not change significantly with the prolongation of sacrifice time. The visual evoked potentials and the number of retinal apoptotic cells in the model group and treatment group were increased gradually (P ＜ 0.05). At the same time point, the number of visual evoked potentials and retinal apoptotic cells in the model group were significantly higher than those in the control group, the visual evoked potential, the number of retinal apoptotic cells in the treatment group were lower than those in the model group (P ＜ 0.05). The RGCs density, optic nerve cholesterol, SIRT1 and HMGCR protein levels in the model group and treatment group were increased gradually with the prolongation of sacrifice time (P ＜ 0.05); at the same time, RGCs density, optic nerve cholesterol, SIRT1 and HMGCR protein levels in the model group were significantly higher than those in the control group, the RGCs density, optic nerve cholesterol, SIRT1 and HMGCR protein levels in the treatment group were lower than those in the model group (P ＜ 0.05). Conclusion Ginsenoside Rg1 has a significant protective effect on optic nerve injury in rats, the mechanism may be related to the up-regulation of the expression of SIRT1 and HMGCR genes and the synthesis of optic nerve cholesterol.
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