Linked Life Data

17161349

Source:http://linkedlifedata.com/resource/pubmed/id/17161349

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13-14
pubmed:dateCreated
2006-12-12
pubmed:abstractText
Bradykinin B1 receptors are exclusively expressed in inflamed tissues. For this reason, they have been related with the outcomes of several pathologies. Ischemia-reperfusion injury is caused by the activation of inflammatory and cytoprotective genes, such as macrophage chemoattractant protein-1 and heme oxygenase-1, respectively. This study was aimed to analyze the involvement of bradykinin B1 and B2 receptors (B1R and B2R) in tissue response after renal ischemia-reperfusion injury. For that, B1R (B1-/-), B2R (B2-/-) knockout animals and its control (wild-type mice, B1B2+/+) were subjected to renal bilateral ischemia, followed by 24, 48 and 120 h of reperfusion. At these time points, blood serum samples were collected for creatinine and urea dosages. Kidneys were harvested for histology and molecular analyses by real-time PCR. At 24 and 48 h of reperfusion, B1-/- group resulted in the lowest serum creatinine and urea levels, indicating less renal damage, which was proved by renal histology. Renal protection associated with B1-/- mice was also related with higher expression of HO-1 and lower expression of MCP-1. In conclusion, the absence of B1R had a protective role against inflammatory responses developed after renal ischemia-reperfusion injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1567-5769
pubmed:author
pubmed:issnType
Print
pubmed:day
20
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1960-5
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Influence of bradykinin B1 and B2 receptors in the immune response triggered by renal ischemia-reperfusion injury.
pubmed:affiliation
Laboratório de Imunologia Clínica e Experimental. Division of Nephrology. Universidade Federal de São Paulo, Escola Paulista de Medicina, São Paulo, Brazil.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't