In vivo protective effect of phosphatidylcholine on carbon tetrachloride induced nephrotoxicity

Phosphatidylcholine (PC) from egg yolk is a bioactive substance with various beneficial effects, including anti-inflammatory and anti-oxidant effects. Recently, this substance has been reported to prevent acute hepatotoxicity. In the present study, we aimed to evaluate the putative protective effect of PC on carbon tetrachloride (CCl₄)-induced nephrotoxicity in ICR mice. Many previous studies demonstrated that CCl₄ induces nephrotoxicity resulting in renal oxidative damage. CCl₄ in corn oil (0.1 ml, 1.2 g/kg) was intra-peritoneally injected into 7-week-old ICR mice twice a week. PC in corn oil (0.1 ml, 100 mg/kg) was then orally injected daily for a week. In 7 days, blood urea nitrogen (BUN) and creatinine concentrations had significantly increased in the CCl₄ group compared to the control group, whereas the PC and CCl₄ co-injected group had significantly decreased BUN and creatinine concentrations compared to the CCl₄ group. Comparative analysis of histopathological injuries revealed that PC abrogated the nephrotoxicity of CCl₄ at 7 days. Accordingly, PC also improved renal fibrosis induced by CCl₄. Various biomarkers associated with oxidative damage appeared to be up-regulated in the CCl₄ group, whereas in the PC and CCl₄ co-injected group, levels of oxidative damage significantly decreased. Aquaporin1 (AQP1), an important water transport protein in the kidney, was down regulated in the CCl₄ group compared to the control group. PC counteracted this effect. These results strongly suggest that PC can protect against oxidative damage induced by CCl₄ in the kidney and enhance recovery from renal disorders.