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Chinese Journal of Immunology ; (12): 1094-1097, 2015.
Artigo em Chinês | WPRIM | ID: wpr-476951

RESUMO

Objective:To study the expression of caspase-3 and free radical injury in hypoxic-ischemic brain damage ( HIBD) of neonatal rats.Methods:All seven-day-old Wistar rats were randomly divided into HIBD group and sham operation group.Brains was obtained at time of 6 h,12 h,24 h,48 h,72 h,96 h after HIBD.Neuronal cell apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling ( TUNEL).The expression level of caspase-3 protein was detected by immunohisto-chemistry.The level of malondialdehyde ( MDA) and supemxide dismutase ( SOD) were measured by thiobarbitic acid colorimetry and xanthin oxidase,respectively.Results:The number of neuronal cell apoptosis and the expression of caspase-3 protein began to increase at 6 h and reached the peak at 48 h in HIBD group,they were both significantly higher than those in the sham operation group at each time point (P<0.05).The level of MDA began to increase at 6 h and reached the peak at 24 h in HIBD group,it was significantly higher than the sham operation group at each time point (P<0.05).The level of SOD began to decrease at 6 h and reached the lowest level at 24 h in HIBD group,it was significantly lower than the sham operation group at each time point ( P<0.05 ) .The number of neuronal cell apoptosis and the expression of caspase-3 protein were positively correlated with the level of MDA, but they were negatively correlated with the level of SOD.Conclusion: Free radical injury promotes the expression of caspase-3 and neuronal cell apoptosis in HIBD.

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