Linked Life Data

19640259

Source:http://linkedlifedata.com/resource/pubmed/id/19640259

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-10-2
pubmed:abstractText
Aristolochic acid nephropathy (AAN) is regarded as a kind of rapidly progressive renal fibrosis caused by the ingestion of herbal remedies containing aristolochic acids (AA). A mouse model of AAN was used to assess the patterns of renal injury and TGF-beta1/Smads signaling pathway during the evolution of tubulointerstitial damage and to relate them to the development of fibrosis. A total of 28 mice were randomly assigned to four groups. Three groups were given aristolochic acid I (AAI) at different doses consecutively by gavage for 30 days, while the control group received only phosphate-buffered saline (PBS). Immunohistochemistry and semi-quantitative reverse transcriptase (RT-PCR) detection of the increased expression of fibroblast marker vimentin and de novo expression of alpha-smooth muscle actin (alpha-SMA) with the loss of epithelial maker cytokeratin 18 (CK18) can be utilized to assess AAI-induced tubular necrosis and extensive cortical interstitial fibrosis in a dose-dependent manner. Transforming growth factor-beta1 (TGF-beta1) has been widely recognized as a key fibrogenic cytokine. In our study, TGF-beta1 in the group at dose of 12 mg/kg/ day AAI increased 109.9% compared to control. Smad2 mRNA level in the group at dose of 4.2 mg/kg/day AAI increased 106.4%, and declined 12% in the group at dose of 12 mg/kg/day AAI; Smad4 expression was down-regulated in experimental groups, which declined 13% in the group at dose of 4.2 mg/kg/day AAI. Smad7 mRNA level was down-regulated by AAI in dose-dependence. Collectively, the involvement in interstitial fibrosis progression of active TGF-beta is highly suggested, via the Smads intracellular signaling pathway. These results may be attributed to the dosage of drug and the treatment of renal interstitial fibrosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1532-4281
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
280-5
pubmed:meshHeading
pubmed-meshheading:19640259-Actins, pubmed-meshheading:19640259-Animals, pubmed-meshheading:19640259-Aristolochic Acids, pubmed-meshheading:19640259-Blotting, Western, pubmed-meshheading:19640259-Cells, Cultured, pubmed-meshheading:19640259-Fibrosis, pubmed-meshheading:19640259-Immunoenzyme Techniques, pubmed-meshheading:19640259-Keratin-18, pubmed-meshheading:19640259-Kidney Tubules, pubmed-meshheading:19640259-Mice, pubmed-meshheading:19640259-Muscle, Smooth, pubmed-meshheading:19640259-Nephritis, Interstitial, pubmed-meshheading:19640259-RNA, Messenger, pubmed-meshheading:19640259-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:19640259-Signal Transduction, pubmed-meshheading:19640259-Smad Proteins, pubmed-meshheading:19640259-Transcription, Genetic, pubmed-meshheading:19640259-Transforming Growth Factor beta1, pubmed-meshheading:19640259-Vimentin
pubmed:year
2009
pubmed:articleTitle
TGF-beta 1/Smads signaling stimulates renal interstitial fibrosis in experimental AAN.
pubmed:affiliation
Laboratory of Pharmacology of the Chinese Veterinary Medicine, Department of Animal Science and Technology, Beijing University of Agriculture, Beijing 102206, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't