Zhonghua fu chan ke za zhi · 2001
[Effect of hypoxia-ischemia on cysteinyl aspartate-specific proteinases activity in cerebral tissue of neonatal rat].
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Wu M, Shi Y
Аннотация
OBJECTIVE: To study the effect of hypoxia-ischemia on cysteinyl aspartate-specific proteinases (caspase-3) activity in cerebral tissue of neonatal rat and probe into its significance.
METHODS: To induce hypoxio-ischemic brain damage (HIBD), the left carotid artery of rats at day 7 was ligated and animals were exposed to 8% oxygen for 2 hours. 0.5, 12, 24, and 48 hours after HIBD, both ipsilateral and contralateral cerebral tissue were ditected and homogenized, caspase-3 activity was measured by cleavage of the colorimetric substrate DEVD-pNA.
RESULTS: Caspase-3 activity in ipsilateral cerebral tissue increased gradually after HIBD and peaked at 24 hours, and then decreased significantly at 48 hours(P < 0.001). There were no significant changes in caspase-3 activity in the contralateral tissue at all time points (P > 0.05).
CONCLUSIONS: Significant activation of caspase-3 after cerebral hypoxia-ischemia strongly suggests that apoptosis is involved in HIBD. Application of caspase inhibitors or other anti-apoptotic agents may become a new therapeutics of HIBD.
METHODS: To induce hypoxio-ischemic brain damage (HIBD), the left carotid artery of rats at day 7 was ligated and animals were exposed to 8% oxygen for 2 hours. 0.5, 12, 24, and 48 hours after HIBD, both ipsilateral and contralateral cerebral tissue were ditected and homogenized, caspase-3 activity was measured by cleavage of the colorimetric substrate DEVD-pNA.
RESULTS: Caspase-3 activity in ipsilateral cerebral tissue increased gradually after HIBD and peaked at 24 hours, and then decreased significantly at 48 hours(P < 0.001). There were no significant changes in caspase-3 activity in the contralateral tissue at all time points (P > 0.05).
CONCLUSIONS: Significant activation of caspase-3 after cerebral hypoxia-ischemia strongly suggests that apoptosis is involved in HIBD. Application of caspase inhibitors or other anti-apoptotic agents may become a new therapeutics of HIBD.