Ginsenoside F2 Intervenes the NF-κB Pathway to Inhibit H2O2-induced Apoptosis
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Abstract:
In this study, the effects of ginsenoside F2 on p65 protein in the NF-κB apoptosis signaling pathway were examined by qRT-PCR and Western blot techniques, and through measuring the effects of ginsenoside F2 on the release rate of lactate dehydrogenase (LDH) and and mitochondrial membrane potential (MMP) of apoptotic cells. It was found that the H2O2 injured cells had a significantly increased LDH release rate (by 42.72%), decreased mitochondrial membrane potential, and decreased relative fluorescence value (by 44.03%), and increased protein and mRNA expression of NF-κB p65 (as 122.73% and 1.66, respectively), compared with the control group (p<0.05). After pretreatment of cells with 1.25, 5, and 20 μmol/L F2, the LDH release rates of the injured group were significantly lowered (p<0.05), to 82.71%, 75.69%, and 69.61% respectively, while the mitochondrial membrane potential values were significantly increased (p<0.05) (with the corresponding relative fluorescence values as 60.22%, 62.76% and 70.96%, respectively). With the increase of F2 concentration, the protein expression of p65 in the NF-κB pathway decreased to 79.49%, 71.92% and 58.39%, respectively (p<0.05), and the mRNA expression was down-regulated to 1.30, 1.18 and 1.01, respectively (p<0.05). The results showed that ginsenoside F2 exhibited an anti-apoptotic effect though reducing the LDH release rate of apoptotic cells, increasing the mitochondrial membrane potential, and inhibiting the activation of NF-κB signaling pathway. This study provides an experimental basis for suppressing effect of ginsenosides on oxidative stress-induced apoptosis.
