title: [Effects and mechanisms of multi-glycoside of Tripterygium wilfordii improving glomerular inflammatory injury by regulating p38MAPK signaling activation in diabetic nephropathy rats].
abstract: OBJECTIVE
  To explore the effects and mechanisms of multi-glycoside of Tripterygium wilfordii (GTW) on improving glomerular inflammatory lesion in rats with diabetic nephropathy (DN).
  
  
  METHODS
  DN model was induced by unilateral nephrectomy and intraperitoneal injection of STZ (35 mg x kg(-1)) twice. The rats were randomly divided into 3 groups, the sham-operated group (Sham group, n = 5), the vehicle-given group (Vehicle group, n = 5 ) and GTW-treated group (GTW group, n = 5). After the model was successfully established, the rats in GTW group were daily oral administrated with GTW suspension (50 mg x kg(-1) x d(-1)), meanwhile, the rats in Vehicle group were daily oral administrated with distilled water (2 mL) for 8 weeks. From the beginning of the administration, all rats were killed 8 weeks later. Blood and renal tissues were collected,and then UAlb, renal function, glomerular morphology characteristics and glomerular macrophages (ED1 + cells) infiltration, as well as the protein expressions of inflammatory cytokines including tumor necrosis factor(TNF)-α and interleukin(IL)-lβ, and the key molecules in p38MAPK signaling pathway including p38 mitogenactivated protein kinase (MAPK), phosphorylated p38 (p-p38MAPK) and transforming growth factor(TGF)-β1 were investigated respectively.
  
  
  RESULTS
  GTW not only ameliorated the general state of health and body weight,but also attenuated UAlb, glomerulosclerosis, the infiltration of glomerular ED1 + cells and the protein expressions of TNF-α, IL-1β, p-p38MAPK and TGF-β1 in the kidney in DN model rats.
  
  
  CONCLUSIONS
  By means of DN model rats, we demonstrated that GTW has the protective effect on renal inflammatory damage in vivo via inhibiting inflammatory cells infiltration and inflammatory cytokines expression. Furthermore, GTW could improve renal inflammatory lesion through down-regulating the expressions of the key signaling molecules in p38MAPK pathway such as p-p38MAPK and TGF-β1 ,and inhibiting the activation of p38MAPK signaling in the kidney.
authors.forename: Yan-Ru
authors.initials: YR
authors.lastname: Huang
authors.forename: Yi-gang
authors.initials: YG
authors.lastname: Wan
authors.forename: Wei
authors.initials: W
authors.lastname: Sun
authors.forename: Zhi-min
authors.initials: ZM
authors.lastname: Mao
authors.forename: Qing
authors.initials: Q
authors.lastname: Zhao
authors.forename: Xi-miao
authors.initials: XM
authors.lastname: Shi
authors.forename: Jian
authors.initials: J
authors.lastname: Yao
mesh_terms: D000818:Animals; D003928:Diabetic Nephropathies / Q000188:drug therapy*; D004195:Disease Models, Animal; D005921:Glomerulonephritis / Q000188:drug therapy*; D006027:Glycosides / Q000494:pharmacology*; D020935:MAP Kinase Signaling System / Q000187:drug effects*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D053773:Transforming Growth Factor beta1 / Q000032:analysis; D029757:Tripterygium / Q000737:chemistry; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology*
chemical_list: D006027:Glycosides; D053773:Transforming Growth Factor beta1; D048051:p38 Mitogen-Activated Protein Kinases