2004•Acta Academiae Medicinae WannanRequires access

Expression of caspase-3 in neuronal apoptosis after intracerebral hemorrhage in rats

Jun Li

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Abstract

Objective To investigate neuronal apoptosis in the region of experimental intracerebral hemorrhage(ICH) in rats and its association with the expression of caspase 3, and to observe the effect of caspase inhibitor zVADfmk on the brain injury after ICH. Methods ICH was induced in rats by injecting stereotactic infusion autologous blood into the caudate nucleus. The male rats were randomly divided into hemorrhage group, sham operation group, zVADfmk treatment group and hemorrhage group which was also divided into several different time point groups. TUNEL method was used to detect apoptosis, and immunohistochemitry method to detect the expression of caspase 3 in cerebral tissues at different time. Results After 6 hours, TUNEL positive cells appeared in the ICH model and were still present for more than 2 weeks after ICH, peaking on the 3rd day. caspase 3 expression preceded apoptosis, increasing obviously after 6 hours, peaking after 24 hours and declining thereafter. The expression of caspase 3 was positively correlated with apoptotic cells(r=0.607, P 0.05) .The quantity of TUNEL positive cells within 3 days after ICH were significantly reduced by treating with caspase inhibitor zVADfmk (P0.05). Conclusion Apoptosis mechanisms may mediate some of the brain injury after ICH. Neuronal apoptosis after ICH is associated with the activation of caspase 3.

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Objective To investigate neuronal apoptosis in the region of experimental intracerebral hemorrhage(ICH) in rats and its association with the expression of caspase 3, and to observe the effect of caspase inhibitor zVADfmk on the brain injury after ICH. Methods ICH was induced in rats by injecting stereotactic infusion autologous blood into the caudate nucleus. The male rats were randomly divided into hemorrhage group, sham operation group, zVADfmk treatment group and hemorrhage group which was also divided into several different time point groups. TUNEL method was used to detect apoptosis, and immunohistochemitry method to detect the expression of caspase 3 in cerebral tissues at different time. Results After 6 hours, TUNEL positive cells appeared in the ICH model and were still present for more than 2 weeks after ICH, peaking on the 3rd day. caspase 3 expression preceded apoptosis, increasing obviously after 6 hours, peaking after 24 hours and declining thereafter. The expression of caspase 3 was positively correlated with apoptotic cells(r=0.607, P 0.05) .The quantity of TUNEL positive cells within 3 days after ICH were significantly reduced by treating with caspase inhibitor zVADfmk (P0.05). Conclusion Apoptosis mechanisms may mediate some of the brain injury after ICH. Neuronal apoptosis after ICH is associated with the activation of caspase 3.

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Available abstract

Objective To investigate neuronal apoptosis in the region of experimental intracerebral hemorrhage(ICH) in rats and its association with the expression of caspase 3, and to observe the effect of caspase inhibitor zVADfmk on the brain injury after ICH. Methods ICH was induced in rats by injecting stereotactic infusion autologous blood into the caudate nucleus. The male rats were randomly divided into hemorrhage group, sham operation group, zVADfmk treatment group and hemorrhage group which was also divided into several different time point groups. TUNEL method was used to detect apoptosis, and immunohistochemitry method to detect the expression of caspase 3 in cerebral tissues at different time. Results After 6 hours, TUNEL positive cells appeared in the ICH model and were still present for more than 2 weeks after ICH, peaking on the 3rd day. caspase 3 expression preceded apoptosis, increasing obviously after 6 hours, peaking after 24 hours and declining thereafter. The expression of caspase 3 was positively correlated with apoptotic cells(r=0.607, P 0.05) .The quantity of TUNEL positive cells within 3 days after ICH were significantly reduced by treating with caspase inhibitor zVADfmk (P0.05). Conclusion Apoptosis mechanisms may mediate some of the brain injury after ICH. Neuronal apoptosis after ICH is associated with the activation of caspase 3.

Key concepts: TUNEL assay, Intracerebral hemorrhage, Apoptosis, Medicine, Caspase 3, Caspase-9, Anesthesia, Pharmacology

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