| Objective:To investigate the effect of sulfated cholecystokinin-8(CCK-8S) on the injury of in vitro cultured dorsal root ganglia(DRG) neurons induced by the nitric oxide donor-sodium nitroprusside(SNP).Methods:Primary cultured DRG neurons were dissected from newborn Sprague-Dawley rats and purified with N2 serum-free medium. At 72 hours after planting, DRG neurons were randomly divided into five groups: normal group; model group(SNP injury)and three experimental groups. The experimental groups were pretreated with different concentration of CCK-8S(group A, 10-8mol/L; group B, 10-7mol/L; group C, 10-6mol/L ) for 30 minutes before injury. All the groups were kept cultivating for 24 hours after injury. Then morphological feature of apoptosis were observed by fluorescence microscope and terminal deoxynucleotidyl transferase-mediated nick end labeling(TUNEL) was used to detect the apoptosis. Immunocytochemistry was used to detect the protein expression of nerve growth factor(NGF) and gorwth associated protein 43(GAP-43). Results:(1) There was no statistical difference in the apoptosis rate of DRG neurons between experimental group A and model group(P>0.05). While the apoptosis rate of DRG neurons in experimental group B and C decreased remarkably compared to model group(P<0.05). And there was negative correlation between the neuron apoptosis rate and the concentration of CCK-8S.(2) There was no statistical difference in protein expression between group A and model group(P>0.05), while protein expression of NGF and GAP-43 were all upregulated in group B and C compared to model group(P<0.05). And there was positive correlation between the protein expression and the concentration of CCK-8S.Conclusion:Our present studies shows that CCK-8S can inhibite the neurotoxicity of nitric oxide and protect DRG neurons from injury induced by SNP. Also CCK-8S can increase the expression of NGF protein and GAP-43 protein after injury, and that may be one of the neuroprotective mechanisms of CCK-8S.
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