Time-dependent enhancement in mitochondrial glutathione status and
ATP generation capacity by schisandrin B treatment decreases the susceptibility
of rat hearts to ischemia-reperfusion injury
Issue title: Proceedings of the Second International
Symposium on Antioxidants in Nutrition and Therapy, Bali, Indonesia, 2–4
October 2002
Affiliations: Department of Biochemistry, The Hong Kong University
of Science & Technology, Clear Water Bay, Hong Kong SAR, China
Note: []
Abstract: In the present study, we examined the time-dependent changes in the
mitochondrial glutathione status and ATP generation capacity in the myocardium
as well as the susceptibility of the myocardium to ischemia-reperfusion (IR)
injury in female Sprague Dawley rats treated with a single pharmacological dose
(1.2 mmol/kg) of schisandrin B (Sch B). Sch B treatment produced a
time-dependent enhancement in myocardial mitochondrial glutathione status, as
evidenced by increases in myocardial mitochondrial reduced glutathione (GSH)
level and activities of glutathione reductase, Se-glutathione peroxidase (GPX)
and glutathione S-transferases, with the response reaching maximum at 48 h
post-dosing and then declining gradually to the control level at 96 h
post-dosing. The enhancement of mitochondrial glutathione status was associated
with an increase in myocardial ATP generation capacity, with the value peaking
at 72 h post-dosing. These beneficial effects of Sch B on the myocardium was
paralleled by a time-dependent decrease in the susceptibility to IR injury,
with the maximum protection demonstrable at 48 h post-dosing. The
cardioprotection was associated with increases in myocardial GSH level and
activities of glutathione antioxidant enzymes (except for GPX whose activity
was suppressed) as well as tissue ATP level/ATP generation capacity. The
results suggest that Sch B treatment can precondition the myocardium by
enhancing the mitochondrial glutathione status and ATP generation capacity,
thereby protecting against IR injury.
Keywords: Schisandrin B, ischemia-reperfusion, myocardium, mitochondrion, glutathione, ATP
Journal: BioFactors, vol. 19, no. 1-2, pp. 43-51, 2003
