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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 5.6mmol/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 10.0μmol/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 (≤1.0μmol/L) significantly increased cell viability in the dose-dependent manner (P<0.05), but apigenin of 10.0μmol/L had no obvious effect on cell viability of high glucose-induced RSC96 cells; apigenin of 1.0μmol/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. [ABSTRACT FROM AUTHOR]

Objective To investigate the effects and mechanisms of secreted protein, acidic and rich in cysteine (SPARC) on high fluoride-induced apoptosis of thyrocytes. Methods Human thyroid cells (Nthy-ori 3-1) were cultured and treated with various concentrations (0.1, 1 and 10mmol/L) of NaF for 24h, and the expression of SPARC was evaluated using Real-time PCR and Western blot, respectively. The cells were divided into four groups: control group, NaF group, si-SPARC group (cells were transfected with SPARC siRNA for 48h and then exposed to NaF for 24h), and si-NC group (cells were transfected with negative control siRNA for 48h and then exposed to NaF for 24h). Cytotoxicity was assayed using CCK-8 and LDH; cell apoptosis rate was detected with ELISA. The expressions of cleaved caspase3 (c-caspase3) and IGF-1R were measured by Western blot. In addition, si-SPARC and si-IGF-1R were co-transfected into thyrocytes to further explore mechanisms of SAPRC by evaluating apoptosis. Results The mRNA and protein levels of SPARC were augmented with the increase of NaF (P<0.05). Cell viability was significantly higher in si-NC group than that in si-SPARC group [(84.02±9.51)% vs. (58.31±6.86)%, P<0.05], and the release rate of LDH was lower [(134.25±18.98)% vs. (195.18±23.50)%, P<0.05]. Cell apoptosis rate was lower in si-SPARC group than that in si-NC group [(124.67±19.44)% vs. (175.24±16.46)%, P<0.05]. In addition, silencing SPARC upregulated the expression of IGF-1R (1.95±0.24 vs. 0.93±0.08, P<0.05), and inhibition of IGF-1R reversed the effect of SPARC on apoptosis. Conclusion Inhibition of SPARC reduces high fluoride-induced cytotoxicity and blocks cell apoptosis. The possible mechanism is through the negative regulation of IGF-1R. [ABSTRACT FROM AUTHOR]