Linked Life Data

17074319

Source:http://linkedlifedata.com/resource/pubmed/id/17074319

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-3
pubmed:dateCreated
2006-11-27
pubmed:abstractText
To explore the protection of emodin on renal dysfunction in the streptozotocin-induced diabetic rats with nephropathy and the role of p38 mitogen-activated protein kinase (p38 MAPK) signal transduction pathway in this protection. 30 male Spraque-Dawley rats were randomly divided into control group, model group and emodin group. The rats in the model group and emodin group were administered with streptozotocin (60 mg/kg) to induce diabetes. 40 mg/kg/day of emodin were orally given to the rats in emodin group. The rats in other groups were only given solvent. Biochemical index were analysed by oxidase and oxidase dynamical enzyme method. Glomerular area and volume were determined quantitatively by using Image Analysis System. Western blotting and immunohistochemical staining was used to detect the total p38 MAPK, phosphorylated p38 MAPK, phosphorylated cAMP response element binding protein (CREB) and fibronectin. The average kidney weight/body weight, glomerular area, glomerular volume and all biochemical indexes significantly increased in model group as compared to the control group (P<0.05), while the average body weight decreased. The expressions of phosphorylaed p38 MAPK, phosphorylated CREB and fibronectin increased by 1.98-fold, 1.94-fold and 1.96-fold respectively in model group compared with those in the control group (P<0.05). Emodin markedly decreased the average kidney weight/body weight, glomerular area, glomerular volume and all biochemical indexes (P<0.05), having a weak action on the level of blood glucose. The expressions of phosphorylated p38 MAPK, phosphorylated CREB and fibronectin also significantly downregulated in emodin group compared with those in model group (P<0.05). Emodin was efficient to ameliorate renal dysfunction in diabetic nephropathy rats probably by its inhibition of the activation of p38 MAPK pathway and downregulation of the expression of fibronectin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0014-2999
pubmed:author
pubmed:issnType
Print
pubmed:day
28
pubmed:volume
553
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
297-303
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17074319-Actins, pubmed-meshheading:17074319-Animals, pubmed-meshheading:17074319-Blood Glucose, pubmed-meshheading:17074319-Blotting, Western, pubmed-meshheading:17074319-Body Weight, pubmed-meshheading:17074319-Cyclic AMP Response Element-Binding Protein, pubmed-meshheading:17074319-Diabetes Mellitus, Experimental, pubmed-meshheading:17074319-Diabetic Nephropathies, pubmed-meshheading:17074319-Emodin, pubmed-meshheading:17074319-Enzyme Inhibitors, pubmed-meshheading:17074319-Fibronectins, pubmed-meshheading:17074319-Immunohistochemistry, pubmed-meshheading:17074319-Kidney, pubmed-meshheading:17074319-Kidney Function Tests, pubmed-meshheading:17074319-Male, pubmed-meshheading:17074319-Organ Size, pubmed-meshheading:17074319-Phosphorylation, pubmed-meshheading:17074319-Rats, pubmed-meshheading:17074319-Rats, Sprague-Dawley, pubmed-meshheading:17074319-Signal Transduction, pubmed-meshheading:17074319-p38 Mitogen-Activated Protein Kinases
pubmed:year
2006
pubmed:articleTitle
Inhibition of phosphorylation of p38 MAPK involved in the protection of nephropathy by emodin in diabetic rats.
pubmed:affiliation
Lab of Pharmacology and Toxicology, School of Pharmaceutical Science, Sun Yat-sen University, Guangzhou, 510080, China.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't