2003Unpublished venueRequires access

The Expression of HSP70 in the Global Cerebral Ischemia Reperfusion and It's Relation to the Ischemic Tolerance

Jun Zhao

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Abstract

Objective: To investigate the expression of heat-shock protein 70 (HSP70) after different periods of global cerebral ischemia in rats and it' s relation to cerebral ischemic tolerance. Methods: In the global cerebral ischemia model with modified 4-vessel occlusion method, detected the expression of HSP70 in hippocampal CA1 region was detected by immunohistochemistry 2 days after brief cerebral global ischemia of 1 min, 2 min, 5 min and 10 min. The histopathological damage in hippocampal CA1 regions were assessed which responsed to secondary lethal ischemic insult 2 days following pretreatment with brief ischemia of 1 min, 2 min, 5 min and 10 min. Results: There is no HSP70 expression in 1 min-ischemia group. The expression of HSP70 appeared in 2 min-group, reached it's maximum in 5 min-group and reduced in 10 min of 4-vessel oclussion. Pretreatment of rats with brief ischemia of 2 min and 5 min produced mild histopathological damage. However, pretreatment with 1 min and 10 min caused severe damage in hippocampal CA1 region. Conclusion: HSP70 is the sensitive marker of cerebral ischemia insult and play a protective role against ischemic injury. This protective effect has a quantity-effect relation in a certain pre-ischemia time window.

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Objective: To investigate the expression of heat-shock protein 70 (HSP70) after different periods of global cerebral ischemia in rats and it' s relation to cerebral ischemic tolerance. Methods: In the global cerebral ischemia model with modified 4-vessel occlusion method, detected the expression of HSP70 in hippocampal CA1 region was detected by immunohistochemistry 2 days after brief cerebral global ischemia of 1 min, 2 min, 5 min and 10 min. The histopathological damage in hippocampal CA1 regions were assessed which responsed to secondary lethal ischemic insult 2 days following pretreatment with brief ischemia of 1 min, 2 min, 5 min and 10 min. Results: There is no HSP70 expression in 1 min-ischemia group. The expression of HSP70 appeared in 2 min-group, reached it's maximum in 5 min-group and reduced in 10 min of 4-vessel oclussion. Pretreatment of rats with brief ischemia of 2 min and 5 min produced mild histopathological damage. However, pretreatment with 1 min and 10 min caused severe damage in hippocampal CA1 region. Conclusion: HSP70 is the sensitive marker of cerebral ischemia insult and play a protective role against ischemic injury. This protective effect has a quantity-effect relation in a certain pre-ischemia time window.

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Available abstract

Objective: To investigate the expression of heat-shock protein 70 (HSP70) after different periods of global cerebral ischemia in rats and it' s relation to cerebral ischemic tolerance. Methods: In the global cerebral ischemia model with modified 4-vessel occlusion method, detected the expression of HSP70 in hippocampal CA1 region was detected by immunohistochemistry 2 days after brief cerebral global ischemia of 1 min, 2 min, 5 min and 10 min. The histopathological damage in hippocampal CA1 regions were assessed which responsed to secondary lethal ischemic insult 2 days following pretreatment with brief ischemia of 1 min, 2 min, 5 min and 10 min. Results: There is no HSP70 expression in 1 min-ischemia group. The expression of HSP70 appeared in 2 min-group, reached it's maximum in 5 min-group and reduced in 10 min of 4-vessel oclussion. Pretreatment of rats with brief ischemia of 2 min and 5 min produced mild histopathological damage. However, pretreatment with 1 min and 10 min caused severe damage in hippocampal CA1 region. Conclusion: HSP70 is the sensitive marker of cerebral ischemia insult and play a protective role against ischemic injury. This protective effect has a quantity-effect relation in a certain pre-ischemia time window.

Key concepts: Ischemia, Hsp70, Hippocampal formation, Medicine, Immunohistochemistry, Heat shock protein, Anesthesia, Occlusion

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