Evaluating the relationship of nitric oxide synthase(NOS)and energy metabolism and cytochrome C and caspase-3 during neuron apoptosis mediated by mitochondria and the protective role of NOS inhibitors.

① Set up fetal rat intrauterine distress model.②Divide into the control group, acute ischemia group, treatment group 1, reperfusion group, treatment group 2.③Measuring expression of caspase-3 and the content of cytochrome C in cytosol.Measuring expression of neuronal nitric oxide synthase(nNOS)mRNA(A)and the activity of inducible nitric oxide synthase(iNOS)and cytochrome oxidase.The change trends of the activity of cytochrome oxidase and the content of cytochrome C and the positive cell number of caspase-3 during different times were analysed.

① The A of NOS(5 min, 15 min)in acute ischemia group was higher than that of treatment group 1(P< 0.05).There was no difference between the A of nNOS(30 min)in two group(P>0.05).But the A of nNOS in two groups was higher than that in the control group(P < 0.05).② iNOS activities in the reperfusion group were all higher than those in the treatment group 2.Both of those in two groups were higher than that in control group(P<0.05).③The activity of mitochondria cytochrome oxidase in the acute ischemia group(5 min, 15 min)were higher than those in the control group(P<0.05).The activity of mitochondria cytochrome oxidase in the acute ischemia group(30 min)was lower than that in the control group(P<0.05).The activity of mitochondria cytochrome oxidase in the treatment groupl(30 min)was higher than that in the acute ischemia group, but lower than that in the control group(P<0.05).The activity of mitochondria cytochrome oxidase in the reperfusion group(6 h, 12 h, 24 h)and the treatment group 2(6 h, 12 h, 24 h)were lower than those in the control group(P < 0.05).The activity of mitochondria cytochrome oxidase in the treatment group 2(6 h, 12 h,24 h)were higher than those in the reperfusion group(P<0.05).④There were no differences between the content of cytochrome C and the positive cell number of caspase-3 in the acute ischemia group(5 min, 15 min)and those in the treatment groupl(P>0.05).The content of cytochrome C and the positive cell number of caspase-3 in the treatment group 1(30 min)were lower than those in the acute ischemia group, but higher than those in the control group(P < 0.05).The content of cytochrome C and the positive cell number of caspase-3 in the reperfusion group(6 h, 12 h,24 h)and the treatment group 2(6 h, 12 h,24 h)were higher than those in the control group(P<0.05).The content of cytochrome C and the positive cell number of caspase-3 in the treatment group 2(6 h, 12 h,24 h)were lower than those in the reperfusion group(P<0.05).

① nNOS and iNOS mediated the damage of cytochrome oxidase's activity and cytochrome C releasing to cytosol and the increase of the expression of caspase-3 during different times of intrauterine distress.② L-NNA play a preventive role in mitochondria energy metabolism failure and neuron apoptosis during acute ischemia stage when intrauterine distress, but effect is limited.AG play a obvious protective role in mitochondria energy metabolism failure and neuron apoptosis when reperfusion following ischemia.