Linked Life Data

18496235

Source:http://linkedlifedata.com/resource/pubmed/id/18496235

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-11-17
pubmed:abstractText
The present study was conducted to assess whether Premarin, a water-soluble estrogen sulfate, can act via estrogen receptors (ERs) to rescue mice from heat-induced lethality. Unanesthetized, unrestrained mice were exposed to ambient temperature of 42.4 degrees C to induce heatstroke (HS). Another group of mice was exposed to room temperature (24 degrees C) and used as normothermic controls. They were given isotonic sodium chloride solution, Premarin (0.1 - 1.0 mg/kg of body weight, i.p.), or Premarin (1 mg/kg of body weight, i.p.) plus the nonselective ER antagonist ICI 182, 780 (0.25 mg/kg of body weight, i.p.) 1 h after the termination of heat stress. Their physiologic and biochemical parameters were continuously monitored. Mice that survived on day 4 of heat treatment were considered survivors. When the vehicle-treated mice underwent heat, the fraction survival and core temperature at +4 h of body heating were found to be 0 of 12 and 34.4 degrees C +/- 3 degrees C, respectively. Administration of Premarin (1 mg/kg) 1 h after the cessation of heat stress rescued the mice from heat-induced death (fraction survival, 12/12) and reduced the hypothermia (core temperature, 37.3 degrees C). The beneficial effects of Premarin in ameliorating lethality and hypothermia can be abolished by simultaneous administration of ICI 182, 780. Both IL-10 (an anti-inflammatory cytokine) and estradiol in the serum were increased significantly in heat-stressed mice administered Premarin compared with vehicle-treated HS group. Heat-induced apoptosis, as indicated by terminal deoxynucleotidyl-transferase-mediated alpha UDP-biotin nick end-labeling staining, in the spleen, liver, and kidney were significantly reduced by Premarin. The increased levels of cellular ischemia (e.g., glutamate, lactate-to-pyruvate ratio, and nitrite) and damage (e.g., glycerol) markers and iNOS expression in the hypothalamus during HS were decreased significantly by Premarin therapy. The levels of proinflammatory cytokines (e.g., IL-1 beta and TNF-alpha) and renal and hepatic dysfunction markers in plasma that are up-regulated in heat stressed mice were significantly lower in Premarin-administered mice. The data indicate that Premarin may act via ERs to rescue mice form HS-induced lethality.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1540-0514
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
30
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
668-74
pubmed:meshHeading
pubmed-meshheading:18496235-Animals, pubmed-meshheading:18496235-Apoptosis, pubmed-meshheading:18496235-Brain, pubmed-meshheading:18496235-Cytokines, pubmed-meshheading:18496235-Dose-Response Relationship, Drug, pubmed-meshheading:18496235-Estradiol, pubmed-meshheading:18496235-Estrogens, Conjugated (USP), pubmed-meshheading:18496235-Female, pubmed-meshheading:18496235-Glutamic Acid, pubmed-meshheading:18496235-Glycerol, pubmed-meshheading:18496235-Heat Stroke, pubmed-meshheading:18496235-Hypothermia, pubmed-meshheading:18496235-Interleukin-10, pubmed-meshheading:18496235-Kidney, pubmed-meshheading:18496235-Liver, pubmed-meshheading:18496235-Mice, pubmed-meshheading:18496235-Pyruvic Acid, pubmed-meshheading:18496235-Receptors, Estrogen, pubmed-meshheading:18496235-Spleen, pubmed-meshheading:18496235-Temperature
pubmed:year
2008
pubmed:articleTitle
Premarin can act via estrogen receptors to rescue mice from heatstroke-induced lethality.
pubmed:affiliation
Department of Urology, Chi Mei Medical Center, Tainan, Taiwan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't