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Objective To investigate the effects of magnesium sulfate on neuron apoptosis and the expressions of caspase-3,bax and bcl-2 after cerebral ischemia-reperfusion injury. Methods Thirty-six gerbils were randomly divided into three groups: Sham-operation group (So,n=12),ischemia-reperfusion group (I-R,n=12) and magnesium sulfate group (Ms,n=12). The neuron apoptosis was detected by the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-fluorescence nick end labeling (TUNEL stain),and the protein expressions of caspase-3,bax and bcl-2 were detected by immunohistochemisty stain.Results Apoptotic neurons and the expressions of caspase-3 and bax were significantly increased in I-R and Ms groups,compared with those in So group. Apoptotic neurons and the expressions of bax and caspase-3 in Ms group were significantly less than those in I-R group. There was no significant difference in the expression of bcl-2 among three groups.Conclusions Magnesium sulfate decreases neuron apoptosis after cerebral ischemia-reperfusion injury,which may be related with the suppressed expressions of caspase-3 and bax.
Objective To investigate the effects of magnesium sulfate on neuron apoptosis and the expressions of caspase-3, bax and bcl-2 after cerebral ischemia-reperfusion injury. Methods Thirty-six gerbils were randomly divided into three groups: Sham-operation group (So, The neuron apoptosis was detected by the terminal deoxynucleotidyl transferase (TdT) -mediated dUTP-fluorescence nick end labeling (n = 12) TUNEL stain), and the protein expressions of caspase-3, bax and bcl-2 were detected by immunohistochemisty stain. Results of Apoptotic neurons and the expressions of caspase-3 and bax were significantly increased in IR and Ms groups, compared with those in so group. Apoptotic neurons and the expressions of bax and caspase-3 in Ms group were significantly less than those in IR group. There was no significant difference in the expression of bcl-2 among three groups. Conclusions Magnesium sulfate decreases neuron apoptosis afte r cerebral ischemia-reperfusion injury, which may be related with the suppressed expressions of caspase-3 and bax.