Pinocembrin Prevents Glutamate-Induced Apoptosis in SH-SY5Y Neuronal Cells Via Decrease of bax/bcl-2 Ratio
European Journal of Pharmacology, Volume 591, Issues 1-3, 4 September 2008, Pages 73-79
Abstract: Pinocembrin is the most abundant flavonoids in propolis, and has been proven to have antioxidant, antibacterial and anti-inflammatory property. To assess the protective effects of pinocembrin on neurons, SH-SY5Y neuronal cells were pretreated with pinocembrin for 2 h followed by co-treatment with glutamate (2 mM) for 12 h…
Treatment with pinocembrin (10− 5, 10− 6, 10− 7 mol/l) increased cell viability dose-dependently, inhibited LDH release and attenuated apoptosis. Intracellular free [Ca2+] was increased after glutamate exposure, and this increase was attenuated in cells treated with pinocembrin. bax mRNA expression increased remarkably following glutamate exposure and pinocembrin treatment manifested a reduction effect. bcl-2 mRNA expression changes were not detected in groups with or without pinocembrin. Western blotting results indicated that pinocembrin treatment reduced the expression of Bax and had no effect on Bcl-2, thus decreased the Bax–Bcl-2 ratio, which is in consistent with the gene expression result. Pinocembrin could also down-regulate the expression of p53 protein, and inhibit the release of cytochrome c from mitochondria to cytosol.
Thus we conclude that pinocembrin exerts its neuroprotective effects in glutamate injury model partly by inhibiting p53 expression, thus Bax–Bcl-2 ratio, and the release of cytochrome c.
Friday, August 22, 2008
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