Apigenin protects schwann cells against the effect of high glucose-induced cell injury through inhibiting NF-κB signal pathway / 西安交通大学学报(医学版)

ABSTRACT

Objective: To investigate the protective effects of apigenin against the cell injury of schwann cells cultured with high glucose so as to provide preliminary experimental basis for treatment of diabetic peripheral neuropathy by apigenin. Methods: RSC96 cells were primarily cultured and randomly divided into three groups respectively treated with 5.6 mmol/L glucose as the control group; with 50mmol /L glucose as high glucose (HG) group; and with HG in the presence of 0.1, 1.0, and 10.0 μmol/L apigenin as Api group. Cell viability of RSC96 cells was detected by CCK-8 assay. Cell apoptosis was detected by flow cytometry. The effects of apigenin on the expression levels of NGF and TNF-α in RSC96 cells cultured with high glucose were detected by ELISA assay. The protein and mRNA expression levels of Bcl-2, Bax, NF-κB, p-NF-κB, and NF-κB were examined by Western blotting and qRT-PCR. Results: Compared with that of HG group, apigenin at low concentrations (≤1.0 μmol/L) significantly increased cell viability in the dose-dependent manner (P<0.05), but apigenin of 10.0 μmol/L had no obvious effect on cell viability of high glucose-induced RSC96 cells; apigenin of 1.0 μmol/L remarkably inhibited high glucose-induced RSC96 cell apoptosis. Apigenin remarkably increased the protein and mRNA expression levels of Bcl-2 in glucose-induced RSC96 cells (P<0.05), but decreased the Bax protein and mRNA expression levels (P<0.05). Moreover, apigenin significantly increased the NGF expression level, and decreased TNF-α expression (P<0.05). In addition, apigenin notably suppressed the phosphorylation level of NF-κB (P<0.05). Conclusion: Apigenin can increase cell viability, inhibit cell apoptosis, and regulate the expression levels of NGF and TNF-α in high glucose-induced schwann cells. Its potential mechanism is possibly related with inhibiting NF-κB signal pathway.