Source:http://linkedlifedata.com/resource/pubmed/id/19695232
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
|
pubmed:dateCreated |
2009-9-8
|
pubmed:abstractText |
The present study found that serum H2S level, H2S production rate, CSE mRNA and CSE protein levels were increased in CVB3-induced myocarditis. dl-proparglygylcine (PAG), an irreversible CSE inhibitor, decreased the infected myocardium titers on postinfection day 4, while NaHS, a H2S donor, alleviated myocardial injury and necrosis, inflammatory cell infiltration and interstitial edema on postinfection day 10. These data reveal that the CSE/H2S pathway is upregulated in the heart in a murine model of CVB3-induced myocarditis and that inhibition of endogenous H2S is beneficial to treatment early in the disease while administration of exogenous H2S is protective to infected myocardium during the later stage.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical | |
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
1090-2104
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:day |
23
|
pubmed:volume |
388
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
595-600
|
pubmed:meshHeading |
pubmed-meshheading:19695232-Animals,
pubmed-meshheading:19695232-Coxsackievirus Infections,
pubmed-meshheading:19695232-Cystathionine gamma-Lyase,
pubmed-meshheading:19695232-Disease Models, Animal,
pubmed-meshheading:19695232-HeLa Cells,
pubmed-meshheading:19695232-Humans,
pubmed-meshheading:19695232-Hydrogen Sulfide,
pubmed-meshheading:19695232-Male,
pubmed-meshheading:19695232-Mice,
pubmed-meshheading:19695232-Mice, Inbred BALB C,
pubmed-meshheading:19695232-Myocarditis
|
pubmed:year |
2009
|
pubmed:articleTitle |
The dual role of the cystathionine gamma-lyase/hydrogen sulfide pathway in CVB3-induced myocarditis in mice.
|
pubmed:affiliation |
Department of Pediatric Cardiology, Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical College, Wenzhou 325027, PR China.
|
pubmed:publicationType |
Journal Article
|