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- Author or Editor: Z.H. Zhang x
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Berberine, a primary pharmacological active constitute of Coptidis Rhizoma, could inhibit neuronal apoptosis in cerebral ischemia. Here, we aimed to investigate whether and how HIF-1 is implicated in the anti-apoptosis effect of berberine on neurons under hypoxia/ischemia. Viability of PC12 cells treated with berberine prior to or following CoCl2-induced hypoxia was evaluated. Annexin V-PI staining was employed to analyse cell apoptosis ratio. HIF-1α and apoptosis-associated molecules were detected via Western blotting. TUNEL and immunohistochemistry were used to demonstrate apoptosis, HIF-1α and p53 levels in cerebral tissue of middle cerebral artery occlusion (MCAO) rats. Berberine pretreatment promoted PC12 cells survival and inhibited apoptosis under hypoxia condition. At the same time, it decreased cell viability and enhancement of apoptosis were observed with berberine treatment under hypoxia. Decreased HIF-1α, caspase 9, caspase 3 and increased Bcl-2/Bax ratio were responsible for the anti-apoptosis of berberine pretreatment. However, pro-apoptosis by berberine under hypoxia was indicated with opposing regulation of those molecules. Significant reduction of apoptosis, HIF-1α and p53 were found in cerebral tissue of MCAO rats treated with berberine. The present study suggests that berberine regulates neuronal apoptosis in cerebral ischemia, which might be dependent on the degree of cell injury. HIF-1 and the followed apoptotic pathway are involved in those effects of berberine.
The aim of the present study was to investigate whether co-administration of nerve growth factor (NGF) and butyrate regulates vanilloid receptor 1 (VR1) and substance P (SP) levels in cultures of rat dorsal root ganglion (DRG) neurons. DRG was dissected out from embryonic 15-day-old Wistar rat and cultured as dissociated cells for 2 days then exposed to NGF (10 ng/ml), butyrate (1 mmol/L), NGF (10 ng/ml) plus butyrate (1 mmol/L) for another 4 days. The neurons cultured continuously in media served as normal control. After that, the cultures were processed for detecting expression of mRNA for VR1 and SP in DRG neurons by RT-PCR, and expression of VR1 protein by Western blot. SP basal release levels were measured by radioimmunoassay (RIA). Capsaicin-evoked SP release was measured by RIA after stimulation with capsaicin (100 nmol/L) for 10 minutes. The neurons exposed to vehicle solution served as vehicle control. Either NGF (10 ng/ml) or butyrate (1 mmol/L) promoted expression of SP mRNA, VR1 mRNA, and VR1 protein in DRG neurons and capsaicin-evoked SP release from DRG neurons. Co-administration of NGF and butyrate showed a synergistic effect on expression of VR1 mRNA, and VR1 protein in DRG neurons and capsaicin-evoked SP release from DRG neurons and a ceiling effect on SP mRNA expression. The elevation of SP mRNA, VR1 mRNA, and VR1 protein promoted by NGF and/or butyrate may be associated with increases of SP release evoked by capsaicin. The mechanisms of the effects of co-administration of NGF and butyrate should be clarified by further study.