Abstract:
AIM:In order to elucidate the molecular mechanism underlying the cardioprotection afforded by schisandrin B (Sch B), the effect of Sch B treatment on the sensitivity of mitochondria to Ca2+-stimulated permeability transition (PT) was investigated in rat hearts under normal and ischemia-reperfusion (I-R) conditions. RESULTS:Myocardial I-R injury caused an increase in the sensitivity of mitochondria to Ca2+-stimulated PT in vitro. The enhanced sensitivity to mitochondrial PT was associated with increases in mitochondrial Ca2+ content as well as the extent of reactive oxidant species production in vitro and cytochrome c release in vivo. The cardioprotection afforded by Sch B pretreatment against I-R-induced injury was paralleled by the decrease in the sensitivity of myocardial mitochondria to Ca2+-stimulated PT, particularly under I-R conditions. CONCLUSION:The results suggest that Sch B treatment increases the resistance of myocardial mitochondria to Ca2+-stimulated PT and protects against I-R-induced tissue injury.
journal_name
Acta Pharmacol Sinjournal_title
Acta pharmacologica Sinicaauthors
Chiu PY,Leung HY,Siu AH,Poon MK,Ko KMdoi
10.1111/j.1745-7254.2007.00614.xsubject
Has Abstractpub_date
2007-10-01 00:00:00pages
1559-65issue
10eissn
1671-4083issn
1745-7254journal_volume
28pub_type
杂志文章abstract:AIM:To establish a 96-well plate based kinase assay using a recombinant vascular endothelial growth factor (VEGF) receptor 1 kinase domain protein. METHODS:A human VEGF receptor 1 kinase domain protein was expressed in E coli, and its activity was monitored by its ability of phosphorylating the polyE4Y substrate coate...
journal_title:Acta pharmacologica Sinica
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doi:
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pub_type: 杂志文章
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更新日期:2002-07-01 00:00:00
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更新日期:2007-10-01 00:00:00
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更新日期:2004-12-01 00:00:00
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更新日期:2003-05-01 00:00:00
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