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.

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.
AuthorsPo Yee Chiu, Kam Ming Ko
JournalBioFactors (Oxford, England) (Biofactors) Vol. 19 Issue 1-2 Pg. 43-51 ( 2003) ISSN: 0951-6433 [Print] Netherlands
PMID14757976 (Publication Type: Journal Article)
Chemical References
  • Antioxidants
  • Cyclooctanes
  • Lignans
  • Polycyclic Compounds
  • schizandrin B
  • Adenosine Triphosphate
  • Glutathione
  • Adenosine Triphosphate (biosynthesis)
  • Animals
  • Antioxidants (chemistry, pharmacology)
  • Cyclooctanes (chemistry, pharmacology)
  • Female
  • Glutathione (metabolism)
  • Heart (drug effects)
  • Lignans (chemistry, pharmacology)
  • Mitochondria, Heart (drug effects, metabolism)
  • Myocardium (metabolism)
  • Polycyclic Compounds (chemistry, pharmacology)
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury (prevention & control)
  • Time Factors

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research network!

Choose Username:
Verify Password: