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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2009-2-9
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pubmed:abstractText |
Acetazolamide has been recognized as an effective treatment for acute mountain sickness. The efficacy of acetazolamide is related to metabolic acidosis, which promotes chemoreceptors to respond to hypoxic stimuli at altitude. In this study, adult male Sprague-Dawley rats were treated with acetazolamide (100mg/kg or 50mg/kg, I.P.) for 3 days. Primary cultured cortical neurons and PC12 cell lines were exposed to acidosis-permissive (pH 6.5) or standard (pH 7.2) media for 20h. HIF-1alpha and its target genes were assayed by Western blot, real-time PCR, HIF-1 DNA-binding assay and chloramphenicol acetyltransferase reporter gene assay. HIF-1alpha protein level and HIF-1 DNA-binding activities were increased in cerebral cortices of rats treated with acetazolamide. Moreover, the mRNA levels of erythropoietin, vascular endothelial growth factor, and glucose transporter-1 also increased. The HIF-1alpha protein level and activity of HIF-driven chloramphenicol acetyltransferase reporters of cortical neurons and PC12 cells treated with acidosis media were significantly enhanced. We conclude that the normoxic induction of HIF-1alpha and HIF-1 mediated genes by acetazolamide may mediate the effect of acetazolamide in the reduction of symptoms of acute mountain sickness.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetazolamide,
http://linkedlifedata.com/resource/pubmed/chemical/Carbonic Anhydrase Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Erythropoietin,
http://linkedlifedata.com/resource/pubmed/chemical/Glucose Transporter Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Hif1a protein, rat,
http://linkedlifedata.com/resource/pubmed/chemical/Hypoxia-Inducible Factor 1, alpha...,
http://linkedlifedata.com/resource/pubmed/chemical/Oxygen,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Endothelial Growth Factor A
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0304-3940
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pubmed:author |
pubmed-author:DouTonghaiT,
pubmed-author:GuGuojunG,
pubmed-author:HaasD JDJ,
pubmed-author:KangZhiminZ,
pubmed-author:LiRunpingR,
pubmed-author:LiuYunY,
pubmed-author:OstrowskiRobert PRP,
pubmed-author:PengZhaoyunZ,
pubmed-author:SunXuejunX,
pubmed-author:TaoHengyiH,
pubmed-author:XuJiajunJ,
pubmed-author:XuWeigangW,
pubmed-author:ZhangJohn HJH
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pubmed:issnType |
Print
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pubmed:day |
27
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pubmed:volume |
451
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
274-8
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pubmed:meshHeading |
pubmed-meshheading:19150486-Acetazolamide,
pubmed-meshheading:19150486-Acidosis, Respiratory,
pubmed-meshheading:19150486-Altitude Sickness,
pubmed-meshheading:19150486-Animals,
pubmed-meshheading:19150486-Anoxia,
pubmed-meshheading:19150486-Carbonic Anhydrase Inhibitors,
pubmed-meshheading:19150486-Cells, Cultured,
pubmed-meshheading:19150486-Cerebral Cortex,
pubmed-meshheading:19150486-DNA-Binding Proteins,
pubmed-meshheading:19150486-Disease Models, Animal,
pubmed-meshheading:19150486-Erythropoietin,
pubmed-meshheading:19150486-Glucose Transporter Type 1,
pubmed-meshheading:19150486-Hypoxia-Inducible Factor 1, alpha Subunit,
pubmed-meshheading:19150486-Male,
pubmed-meshheading:19150486-Oxygen,
pubmed-meshheading:19150486-PC12 Cells,
pubmed-meshheading:19150486-RNA, Messenger,
pubmed-meshheading:19150486-Rats,
pubmed-meshheading:19150486-Rats, Sprague-Dawley,
pubmed-meshheading:19150486-Up-Regulation,
pubmed-meshheading:19150486-Vascular Endothelial Growth Factor A
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pubmed:year |
2009
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pubmed:articleTitle |
Normoxic induction of cerebral HIF-1alpha by acetazolamide in rats: role of acidosis.
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pubmed:affiliation |
Department of Diving Medicine, Second Military Medical University, Shanghai 200433, People's Republic of China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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