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1.
Journal of Southern Medical University ; (12): 263-265, 2010.
Article in Chinese | WPRIM | ID: wpr-269577

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of co-exposure to hyperthermia and lipopolysaccharides (LPS) on tumor necrosis factor-alpha (TNF-alpha) expression in the lungs and small intestines of rats.</p><p><b>METHODS</b>Male pathogen-free Wistar rats were randomly assigned into saline-injected normothermic control (C), saline heat exposure (H), LPS normothermic control (L), and LPS plus heat exposure (HL) groups. The rats in H and HL groups were exposed in a chamber at an ambient dry bulb temperature (Tdb) of 35.0-/+0.5 degrees celsius;, and those in C and L groups to 26-/+0.5 degrees celsius;. In L and HL groups, the rats were given an intravenous injection of LPS 10 mg/kg via the tail vein to induce endotoxemia, and those in C and H group received 10 ml/kg injection. The plasma levels of sTNFrI and sTNFrII were detected at different time points using ELISA. The expression of TNF-alpha in the lungs and small intestines was detected by immunohistochemical SABC method, and the damage of the lungs and small intestines evaluated histologically 120 min after the treatment.</p><p><b>RESULTS</b>Co-exposure to hyperthermia and LPS caused significantly enhanced expressions of TNF-alpha and its receptor sTNFrI and sTNFrII in the plasma and tissues and obvious histopathological damage in the lung and small intestines.</p><p><b>CONCLUSION</b>Co-stress of hyperthermia and LPS-induced toxicity is associated with the expression of TNF-alpha in the lung and small intestines.</p>


Subject(s)
Animals , Male , Rats , Fever , Metabolism , Hot Temperature , Immunohistochemistry , Intestine, Small , Metabolism , Lipopolysaccharides , Lung , Metabolism , Random Allocation , Rats, Wistar , Stress, Physiological , Tumor Necrosis Factor-alpha , Metabolism
2.
Journal of Southern Medical University ; (12): 1629-1631, 2009.
Article in Chinese | WPRIM | ID: wpr-282630

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the effects of co-exposure of LPS and heat on TNF-alpha expression in rat kidneys.</p><p><b>METHODS</b>Male pathogen-free Wistar rats were randomly assigned in saline-injected normothermic control (C group), saline-injected heat exposure (H group), LPS-injected normothermic control (L group), and LPS-injected heat exposure (HL group). The rats in H and HL groups were exposed in a chamber at an ambient dry bulb temperature (Tdb) of 35.0-/+0.5 degrees, and those in C and L groups were exposed to a Tdb of 26-/+0.5 degrees. The rats in L and HL groups were given an intravenous injection of LPS (10 mg/kg) via the tail vein to induce endotoxemia, and equivalent normal saline was injected in C and H groups. TNF-alpha expression in the kidney was detected by immunohistochemical SABC method, and the renal damage was evaluated histologically at 120 min after the treatment.</p><p><b>RESULTS</b>Co-exposure of the rats with LPS and heat caused significantly enhanced TNF-alpha expression and histopathological damage in the kidneys.</p><p><b>CONCLUSION</b>LPS combined with heat exposure causes renal toxicity, while is closely associated with the expression of TNF-alpha in the kidneys.</p>


Subject(s)
Animals , Male , Rats , Gene Expression Regulation , Hot Temperature , Immunohistochemistry , Interleukins , Metabolism , Kidney , Metabolism , Pathology , Lipopolysaccharides , Pharmacology , Rats, Wistar , Stress, Physiological , Tumor Necrosis Factor-alpha , Metabolism
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