CCK-8 prevents glutamate-induced apoptosis in cultured cortical neurons via up-regulation of bcl-2/bax ratio and down-regulation of caspase-3 / 重庆医科大学学报
Journal of Chongqing Medical University
; (12)2007.
Article
in Zh
| WPRIM
| ID: wpr-581314
Responsible library:
WPRO
ABSTRACT
Objective:
To investigate the mechanisms responsible for the neuroprotection by cholecystokinin octapeptide against glutamate-induced apoptosis in vitro cultured cortical neurons.Methods:
Primary cultured corticaI neurons from SD rats of 0~24 hold were incubated for 8 days. The cultured cells were divided randomly into three groups control group,glutamate group and CCK group. In the controI group,cells were not treated with glutamate orCCK;Neurons in glutamate group were incubated with 50?mol/Lglutamate for 30 min;In CCK group,CCK-8 was added to the Neurons 24 h prior to incubation with glutamate. After injuried by glutamate,cells in all the groups were incubated with normal medium for 0,6,12,24 h and 48 h. At the five time points,cells were fixed respectively for experiment. Cell viability were determined by the colorimetric MTT assay;The protein expression of Bcl-2,Bax and Caspase-3 were determined by immunocytochemistry techniques.Results:
Pretreatment with CCK for 24 h significantly improved glutamate-induced suppression of cell viability. Pretreatment with CCK also completely reversed the suppression of Bcl-2 expression,and significantly inhibited Bax overexpression and Caspase-3 activition induced by glutamate.Conclusion:
Theneuroprotective mechanisms of CCK against glutamate-induced apoptosis in cultured cortical neurons may be associated with up-regulation of Bcl-2/Bax ratio and down-regulation of Caspase-3.
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Index:
WPRIM
Language:
Zh
Journal:
Journal of Chongqing Medical University
Year:
2007
Type:
Article