Protective Effect of Ginsenosides Rg3 Against Nerve Cell Injury Induced by Oxidative Stress
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Abstract:
To determine protective effect of ginsenoside Rg3 on oxidative stress-induced injury in PC12 cells, the inhibitory effect of Rg3 on oxygen free radicals induced cell oxidation was detected in a cellular antioxidant activity experiment. To this end, an oxidative stress model of PC12 cells induced by H2O2 was established, whose cell viability was detected using the CCK-8 method. The effects of Rg3 on the protein expression of p65 and CREB, related to inflammatory and apoptosis, were detected by western blotting. The results showed that the antioxidant ability of Rg3 in response to oxygen free radicals was approximately 7.3-fold that of Trolox. Cell viability was decreased by 60.11% after treatment with 200 μmol/L H2O2. Meanwhile, the relative expression of p-p65 protein was increased to 1.30, and p-CREB protein was decreased to 0.80. The cell viabilities of protective groups pretreated with different concentrations of Rg3 (10, 20, and 40 μmol/L) were found to increase by 74.00%, 76.04%, and 80.36%, respectively. The relative expressions of p-p65 protein decreased to 1.18, 1.03, and 0.82, respectively. Meanwhile, the relative expression of p-CREB protein increased to 1.31, 1.75 and 2.30, respectively. These results suggest that ginsenoside Rg3 may protect PC12 cells from oxidative damage by scavenging oxygen free radicals. The underlying mechanisms may be related to the NF-κB/CREB pathway, which reduces inflammation and apoptosis in PC12 cells, thereby inhibiting the oxidative stress-induced nerve cell damage. These findings provide a theoretical basis for the study of the neurotrophic characteristics of ginseng and the development of related functional foods.