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.
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This work was supported by a RGC grant (HKUST 6122/04M) from the Research Grants Council, Hong Kong.
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Chiu, Py., Leung, Hy., Siu, A. et al. Schisandrin B decreases the sensitivity of mitochondria to calcium ion-induced permeability transition and protects against ischemia-reperfusion injury in rat hearts. Acta Pharmacol Sin 28, 1559–1565 (2007). https://doi.org/10.1111/j.1745-7254.2007.00614.x
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DOI: https://doi.org/10.1111/j.1745-7254.2007.00614.x
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