2007Journal of Shandong UniversityRequires access

Effects of caspase-3 activation and cytochrome c release in cerebral ischemia reperfusion injury

WU Cheng-yua

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Abstract

Objective To evaluate the effects of caspase-3 activation and cytochrome c release in cerebral ischemia reperfusion induced neuronal cell death.Methods A focal cerebral ischemia C57L mice model was established by the middle cerebral occlusion(MACo)method.Caspase-3 activity was determined by an enzyme activity assay at different time points after ischemia reperfusion.Caspase-3 activation and cytochrome c release were determined by immunohistological staining and Western blot.Results ①Caspase-3 activation immediately occurred at 3 h after ischemia reperfusion and was gradually increased to a peak at 12 h to 24 h.②Caspase-3 was significantly activated at 6 h after completion of ischemia reperfusion and it was increased by 7.6 times in comparison with the sham control(P0.01).③Cytochrome c release occurred at 6h after completion of ischemia reperfusion and it was increased by 8.5 times in comparison with the sham control(P0.01).Conclusions Caspase-3 activation and cytochrome c release play a critical role in neuronal cell death induced by cerebral ischemeia reperfusion.This stuely provides insights into the mechanism of events involved in ischmeia reperfusion injury.

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Objective To evaluate the effects of caspase-3 activation and cytochrome c release in cerebral ischemia reperfusion induced neuronal cell death.Methods A focal cerebral ischemia C57L mice model was established by the middle cerebral occlusion(MACo)method.Caspase-3 activity was determined by an enzyme activity assay at different time points after ischemia reperfusion.Caspase-3 activation and cytochrome c release were determined by immunohistological staining and Western blot.Results ①Caspase-3 activation immediately occurred at 3 h after ischemia reperfusion and was gradually increased to a peak at 12 h to 24 h.②Caspase-3 was significantly activated at 6 h after completion of ischemia reperfusion and it was increased by 7.6 times in comparison with the sham control(P0.01).③Cytochrome c release occurred at 6h after completion of ischemia reperfusion and it was increased by 8.5 times in comparison with the sham control(P0.01).Conclusions Caspase-3 activation and cytochrome c release play a critical role in neuronal cell death induced by cerebral ischemeia reperfusion.This stuely provides insights into the mechanism of events involved in ischmeia reperfusion injury.

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Available abstract

Objective To evaluate the effects of caspase-3 activation and cytochrome c release in cerebral ischemia reperfusion induced neuronal cell death.Methods A focal cerebral ischemia C57L mice model was established by the middle cerebral occlusion(MACo)method.Caspase-3 activity was determined by an enzyme activity assay at different time points after ischemia reperfusion.Caspase-3 activation and cytochrome c release were determined by immunohistological staining and Western blot.Results ①Caspase-3 activation immediately occurred at 3 h after ischemia reperfusion and was gradually increased to a peak at 12 h to 24 h.②Caspase-3 was significantly activated at 6 h after completion of ischemia reperfusion and it was increased by 7.6 times in comparison with the sham control(P0.01).③Cytochrome c release occurred at 6h after completion of ischemia reperfusion and it was increased by 8.5 times in comparison with the sham control(P0.01).Conclusions Caspase-3 activation and cytochrome c release play a critical role in neuronal cell death induced by cerebral ischemeia reperfusion.This stuely provides insights into the mechanism of events involved in ischmeia reperfusion injury.

Key concepts: Ischemia, Cytochrome c, Reperfusion injury, Western blot, Apoptosis, Pharmacology, Caspase 3, Cytochrome

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