Schisandrin B modulates the ischemia-reperfusion induced changes in non-enzymatic antioxidant levels in isolated-perfused rat hearts.
Isolated Langendorff-perfused rat hearts were subjected to a fixed period of ischemia followed by increasing periods of reperfusion for investigating the changes in the extent of ischemia-reperfusion (IR) injury and tissue levels of non-enzymatic antioxidants. Effects of schisandrin B (Sch B) and (+/-) alpha-lipoic acid (LA) pretreatment were also examined. A 40-min of ischemia (40-I) followed by 20- or 40-min of reperfusion (20-R or 40-R) caused sustainable tissue damage in isolated hearts, as indicated by the increased extent of lactate dehydrogenase (LDH) leakage and impaired contractile force. The myocardial IR injury was associated with a marked decrease in tissue ascorbic acid (V(C)) level. However, myocardial reduced glutathione (GSH) and alpha-tocopherol (V(E)) levels remained relatively unchanged except under a more severe IR condition (40-I, 40-R). Pretreating rats with Sch B or LA at a daily dose of 1.2 mmol/kg for 3 days protected against IR injury in isolated hearts to varying degrees. While only Sch B pretreatment could improve the recovery of contractile force, LA pretreatment produced a better inhibitory effect on LDH leakage. The protection against IR injury was associated with significant increases in myocardial V(E) and V(C) levels in both Sch B and LA pretreated hearts. The ensemble of results suggests that the cardioprotection afforded by Sch B or LA pretreatment may at least in part be attributed to the modulation on the interplay among non-enzymatic antioxidants under oxidative stress induced by IR.
Ko
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Department of Biochemistry, The Hong Kong University of Science and Technology, Kowloon, China.
Yiu
H Y
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D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001205:Ascorbic Acid / Q000378:metabolism; D034242:Cyclooctanes; D005260:Female; D006321:Heart / Q000502:physiology*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D017705:Lignans / Q000494:pharmacology*; D008297:Male; D008956:Models, Chemical; D009206:Myocardium / Q000166:cytology* / Q000378:metabolism*; D018384:Oxidative Stress; D010477:Perfusion; D011083:Polycyclic Compounds / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000517:prevention & control*; D008063:Thioctic Acid / Q000494:pharmacology; D013997:Time Factors
D000975:Antioxidants; D034242:Cyclooctanes; D017705:Lignans; D011083:Polycyclic Compounds; C015499:schizandrin B; D008063:Thioctic Acid; D007770:L-Lactate Dehydrogenase; D001205:Ascorbic Acid