Attenuation of ureteral obstruction-induced renal injury by polyenylphosphatidylcholine

• Published in: International journal of urology Vol. 14; no. 4; pp. 350 - 356
• Main Authors: Akin, Melih, Demirbilek, Savas, AY, Selma, Gurunluoglu, Kubilay, Turkmen, Emine, Tas, Erkan, Aksoy, Rauf Tugrul, Baykarabulut, Aysun, Edali, Mehmet Naci
• Format: Journal Article
• Language: English
• Published: Melbourne, Australia Blackwell Publishing Asia 01-04-2007
• Subjects: Actins - metabolism; alpha smooth muscle actin; Animals; Cytokines - metabolism; Disease Models, Animal; Female; Kidney Diseases - etiology; Kidney Diseases - pathology; Kidney Diseases - prevention & control; Leukocyte Count; Lipid Peroxidation - physiology; NF-kappa B - metabolism; nuclear factor kappa beta; Oxidative Stress - physiology; Phosphatidylcholines - therapeutic use; polyenylphosphatidylcholine; Rats; Rats, Wistar; transforming growth factor-beta1; unilateral ureteral obstruction; Ureteral Obstruction - complications; Ureteral Obstruction - metabolism; Ureteral Obstruction - pathology
• ISSN: 0919-8172; 1442-2042
• DOI: 10.1111/j.1442-2042.2006.01717.x

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 (TGFβ‐1), alpha smooth muscle actin (α‐SMA) and nuclear factor kappa beta (NF‐κβ) 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, TGFβ‐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 TGFβ‐1 levels and also decreased expressions of α‐SMA and NF‐κβ. 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.