Effect of heat stress on lipopolysaccharide-induced vascular permeability change in mice
Autor: | Takamura Muraki, Toshimasa Yoshioka, Emiko Fujii, Taiyo Suganuma, Kaoru Irie |
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Rok vydání: | 2002 |
Předmět: |
Lipopolysaccharides
Male Salmonella typhimurium medicine.medical_specialty Lipopolysaccharide Fever Lactams Macrocyclic Blotting Western Vascular permeability Cysteine Proteinase Inhibitors Heat Stress Disorders Guanidines Dinoprostone Hsp90 inhibitor Capillary Permeability chemistry.chemical_compound Mice Heat shock protein Internal medicine medicine Benzoquinones Animals RNA Messenger Prostaglandin E2 Heat-Shock Proteins Skin Pharmacology biology Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha Quinones Hsp90 Hsp70 Isoenzymes Endocrinology chemistry Cyclooxygenase 2 Prostaglandin-Endoperoxide Synthases Immunology biology.protein Molecular Medicine Tumor necrosis factor alpha medicine.drug |
Zdroj: | The Journal of pharmacology and experimental therapeutics. 303(2) |
ISSN: | 0022-3565 |
Popis: | The effect of heat shock protein (hsp) induction on lipopolysaccharide (LPS)-induced increase in vascular permeability was studied in mice as a model of inflammatory mediator-induced inflammatory response. Mice were exposed to an ambient temperature of 43 degrees C for 1 h and then returned to 23 degrees C to recover up to 24 h. Dermal contents of hsp70 and hsp90 but not heat shock cognate protein (hsc)70 increased at 6 h after heat exposure and returned to the basal level at 24 h. LPS was injected subcutaneously at 0, 2, 4, 6, or 24 h after heat exposure. Two hours after LPS injection, vascular permeability was assessed by dermal accumulation of intravenously injected dye. LPS-induced dye leakage was reduced by 42 and 49% in heat-exposed mice after recovery for 4 and 6 h, respectively. Increases in dermal tumor necrosis factor-alpha (TNF-alpha) and prostaglandin E(2) (PGE(2)) contents induced by LPS were significantly reduced in the heat-stressed mice recovered for 6 h. LPS-induced increase in cyclooxygenase-2 but not TNF-alpha mRNA was attenuated in heat-stressed mice. Deoxyspergualin, an inhibitor of hsc70 and hsp90, and geldanamycin, a specific hsp90 inhibitor, dose dependently reversed the inhibitory effect of heat stress on LPS-induced dye leakage and dermal TNF-alpha content but not PGE(2) content. These results suggest that heat stress attenuated LPS-induced vascular permeability change by inducing hsp90, leading to inhibition of TNF-alpha production. |
Databáze: | OpenAIRE |
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