Abstract
Effects of hypoxia ischemia on caspase-3 expression and neuronal apoptosis in the brain of neonatal mice were investigated. Twenty-five neonatal CD1 mice aged 1 week were selected and randomly divided into sham-operation group (n=8) and newborn hypoxia ischemia encephalopathy (NHIE) model group (n=17). The messenger ribonucleic acid (mRNA) expression levels of caspase-3 and Fas ligand (FasL) in brain tissues of mice in both groups were detected via reverse transcription-polymerase chain reaction (RT-PCR). The protein expression levels of caspase-3 and FasL in mice in both groups were detected via western blotting. Moreover, apoptosis of brain tissues was detected using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), and caspase-3 protein expression level in brain tissues was detected using immunohistochemical methods. Results of RT-PCR and western blotting revealed that compared with those in sham-operation group, caspase-3 and FasL expression levels in model group were significantly increased. Results of TUNEL showed that the number of apoptotic neurons in model group was significantly increased. Besides, results of immunohistochemical detection manifested that the caspase-3 protein expression level in model group was obviously increased. Hypoxia ischemia can lead to significant increase of caspase-3 expression and increase of neuronal apoptosis in the brain of neonatal mice.