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Neuronal apoptosis and expression of caspase-12 mRNA and protein following focal cerebral ischemia-reperfusion in rats

Yanyan Liu

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Abstract

Aim To study the expression of caspase-12 mRNA and protein following focal cerebral ischemia-reperfusion in rats,and explore the effect of endoplasmic reticulum pathway on neuronal apoptosis.Methods 60 male Wistar rats were randomly divided into sham-operated group and ischemic group.The middle cerebral artery occlusion(MCAO)models were established by using the intraluminal suture occlusion method,neuronal apoptosis was detected by TUNEL staining,the expression of caspase-12 protein was detected by immunohistochemical staining,the expression of caspase-12 mRNA was detected by RT-PCR method.Results In ischemic group,the number of apoptotic cells and the expression of caspase-12 mRNA and protein were gradually increased following prolonged cerebral reperfusion,reached the peak at 24 h.The number of apoptotic cells and the expression of caspase-12 mRNA and protein in ischemic group were significantly less than those of sham-operated group at all times(P0.01).Conclusion The number of apoptotic cells and the expression of caspase-12 mRNA and protein increased significantly following focal cerebral ischemia-reperfusion,which indicated endoplasmic reticulum pathway might be involved in regulating neuronal apoptosis following cerebral ischemia-reperfusion.

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Aim To study the expression of caspase-12 mRNA and protein following focal cerebral ischemia-reperfusion in rats,and explore the effect of endoplasmic reticulum pathway on neuronal apoptosis.Methods 60 male Wistar rats were randomly divided into sham-operated group and ischemic group.The middle cerebral artery occlusion(MCAO)models were established by using the intraluminal suture occlusion method,neuronal apoptosis was detected by TUNEL staining,the expression of caspase-12 protein was detected by immunohistochemical staining,the expression of caspase-12 mRNA was detected by RT-PCR method.Results In ischemic group,the number of apoptotic cells and the expression of caspase-12 mRNA and protein were gradually increased following prolonged cerebral reperfusion,reached the peak at 24 h.The number of apoptotic cells and the expression of caspase-12 mRNA and protein in ischemic group were significantly less than those of sham-operated group at all times(P0.01).Conclusion The number of apoptotic cells and the expression of caspase-12 mRNA and protein increased significantly following focal cerebral ischemia-reperfusion,which indicated endoplasmic reticulum pathway might be involved in regulating neuronal apoptosis following cerebral ischemia-reperfusion.

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Available abstract

Aim To study the expression of caspase-12 mRNA and protein following focal cerebral ischemia-reperfusion in rats,and explore the effect of endoplasmic reticulum pathway on neuronal apoptosis.Methods 60 male Wistar rats were randomly divided into sham-operated group and ischemic group.The middle cerebral artery occlusion(MCAO)models were established by using the intraluminal suture occlusion method,neuronal apoptosis was detected by TUNEL staining,the expression of caspase-12 protein was detected by immunohistochemical staining,the expression of caspase-12 mRNA was detected by RT-PCR method.Results In ischemic group,the number of apoptotic cells and the expression of caspase-12 mRNA and protein were gradually increased following prolonged cerebral reperfusion,reached the peak at 24 h.The number of apoptotic cells and the expression of caspase-12 mRNA and protein in ischemic group were significantly less than those of sham-operated group at all times(P0.01).Conclusion The number of apoptotic cells and the expression of caspase-12 mRNA and protein increased significantly following focal cerebral ischemia-reperfusion,which indicated endoplasmic reticulum pathway might be involved in regulating neuronal apoptosis following cerebral ischemia-reperfusion.

Key concepts: Apoptosis, Ischemia, Messenger RNA, TUNEL assay, Endoplasmic reticulum, Caspase 3, Immunohistochemistry, Middle cerebral artery

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