Regulation of thermotolerance and ischemic tolerance.
Thermotolerance and ischemic tolerance are two major biological aspects where heat shock (stress) proteins exert essential roles for survival in cells as well as in various tissues. Bioflavonoids prevent the cells from acquiring thermotolerance after stresses through specific inhibition in the induction of heat shock proteins. The mechanism of this inhibition is revealed to be due to the prevention of the activation of heat shock factor 1 after heat shock. The induction of stress proteins during the ischemic stress is then described in global as well as focal cerebral ischemic model in rats. The activation of heat shock factor 1 after ischemia is first shown to induce various stress proteins in the central nervous system.
Nagata
K
K
Department of Cell Biology, Kyoto University, Japan.
D001921:Brain / Q000378:metabolism; D004268:DNA-Binding Proteins / Q000378:metabolism; D015180:Electrophoresis, Gel, Two-Dimensional; D005419:Flavonoids / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects; D006360:Heat-Shock Proteins / Q000378:metabolism*; D006358:Hot Temperature; D006801:Humans; D007511:Ischemia / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D011794:Quercetin / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D013312:Stress, Physiological
D004268:DNA-Binding Proteins; D005419:Flavonoids; D006360:Heat-Shock Proteins; D012333:RNA, Messenger; D011794:Quercetin