Source:http://linkedlifedata.com/resource/pubmed/id/14757976
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0001480,
umls-concept:C0012655,
umls-concept:C0017817,
umls-concept:C0035126,
umls-concept:C0074175,
umls-concept:C0079411,
umls-concept:C0087111,
umls-concept:C0449438,
umls-concept:C0521451,
umls-concept:C0547047,
umls-concept:C1516240,
umls-concept:C1627358,
umls-concept:C1882687,
umls-concept:C2349975
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pubmed:issue |
1-2
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pubmed:dateCreated |
2004-2-3
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pubmed:abstractText |
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.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclooctanes,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione,
http://linkedlifedata.com/resource/pubmed/chemical/Lignans,
http://linkedlifedata.com/resource/pubmed/chemical/Polycyclic Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/schizandrin B
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pubmed:status |
MEDLINE
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pubmed:issn |
0951-6433
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
19
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
43-51
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pubmed:dateRevised |
2004-11-17
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pubmed:meshHeading |
pubmed-meshheading:14757976-Adenosine Triphosphate,
pubmed-meshheading:14757976-Animals,
pubmed-meshheading:14757976-Antioxidants,
pubmed-meshheading:14757976-Cyclooctanes,
pubmed-meshheading:14757976-Female,
pubmed-meshheading:14757976-Glutathione,
pubmed-meshheading:14757976-Heart,
pubmed-meshheading:14757976-Lignans,
pubmed-meshheading:14757976-Mitochondria, Heart,
pubmed-meshheading:14757976-Myocardium,
pubmed-meshheading:14757976-Polycyclic Compounds,
pubmed-meshheading:14757976-Rats,
pubmed-meshheading:14757976-Rats, Sprague-Dawley,
pubmed-meshheading:14757976-Reperfusion Injury,
pubmed-meshheading:14757976-Time Factors
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pubmed:year |
2003
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pubmed:articleTitle |
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.
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pubmed:affiliation |
Department of Biochemistry, The Hong Kong University of Science & Technology, Clear Water Bay, Hong Kong SAR, China.
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pubmed:publicationType |
Journal Article
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