title: Attenuation of ureteral obstruction-induced renal injury by polyenylphosphatidylcholine.
abstract: BACKGROUND
  The cytoprotective, antioxidant and antifibrotic effects of polyenylphosphatidylcholine (lecithin, PPC) have been demonstrated both experimentally and clinically. The present study investigated whether PPC treatment has any beneficial effect on renal injury in unilateral partial ureteral obstruction (UUO) in rats.
  
  
  METHODS
  Forty Wistar-Albino rats were split into three groups (sham-operated controls, untreated and treated rats). Rats of the untreated and treated groups (n = 15) underwent UUO with two-thirds of the left ureter embedded in the psoas muscle. In group 3, PPC was given orally at a dose of 100 mg/day for 30 days. At the end of the 30th day of the experimental period, obstructed kidneys and blood samples were harvested. To investigate the therapeutic efficacy of PPC treatment in UUO kidneys, oxidant and antioxidant enzyme levels, lipid peroxidation, proinflammatory cytokines (interleukin-1, interleukin-6, tumor necrosis factor alpha), transforming growth factor beta-1 (TGFbeta-1), alpha smooth muscle actin (alpha-SMA) and nuclear factor kappa beta (NF-kappabeta) expression, leukocyte infiltration (ED1, ED2, CD4 and CD8 immunohistochemistry), and tubulointerstitial damage in the obstructed kidneys were studied.
  
  
  RESULTS
  Oxidative stress, neutrophil infiltration, release of cytotoxic mediators, TGFbeta-1 levels, tubulointerstitial damage, alpha-SMA and NF-KB expressions in kidney tissue were significantly increased in the UUO rats. PPC treatment attenuated oxidative stress, leukocyte infiltration, cytotoxic mediator, and TGFbeta-1 levels and also decreased expressions of alpha-SMA and NF-kappabeta. It was associated with decreased tubulointerstitial damage, compared with UUO alone.
  
  
  CONCLUSIONS
  These results indicate that PPC treatment protects against UUO-induced renal injury in rats possibly through its antioxidant, anti-inflammatory and antifibrotic actions.
authors.affiliation: Department of Pediatric Surgery, School of Medicine, Inonu University, Malatya, Turkey.
authors.forename: Melih
authors.initials: M
authors.lastname: Akin
authors.forename: Savas
authors.initials: S
authors.lastname: Demirbilek
authors.forename: Selma
authors.initials: S
authors.lastname: Ay
authors.forename: Kubilay
authors.initials: K
authors.lastname: Gurunluoglu
authors.forename: Emine
authors.initials: E
authors.lastname: Turkmen
authors.forename: Erkan
authors.initials: E
authors.lastname: Tas
authors.forename: Rauf Tugrul
authors.initials: RT
authors.lastname: Aksoy
authors.forename: Aysun
authors.initials: A
authors.lastname: Baykarabulut
authors.forename: Mehmet Naci
authors.initials: MN
authors.lastname: Edali
mesh_terms: D000199:Actins / Q000378:metabolism; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D007674:Kidney Diseases / Q000209:etiology* / Q000473:pathology / Q000517:prevention & control*; D007958:Leukocyte Count; D015227:Lipid Peroxidation / Q000502:physiology; D016328:NF-kappa B / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D010713:Phosphatidylcholines / Q000627:therapeutic use*; D051381:Rats; D017208:Rats, Wistar; D014517:Ureteral Obstruction / Q000150:complications* / Q000378:metabolism / Q000473:pathology
chemical_list: D000199:Actins; D016207:Cytokines; D016328:NF-kappa B; D010713:Phosphatidylcholines; C005152:lipostabil