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...

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Published in:Experimental and toxicologic pathology : official journal of the Gesellschaft für Toxikologische Pathologie 2016-11, Vol.68 (10), p.553-558
Main Authors: Kim, Sokho, Na, Ji-Young, Song, Kibbeum, Kwon, Jungkee
Format: Article
Language:English
Subjects:
Animals
Antioxidants - pharmacology
Aquaporin1
Carbon tetrachloride
Carbon Tetrachloride Poisoning - prevention & control
Disease Models, Animal
Immunoblotting
Kidney - drug effects
Kidney - pathology
Male
Mice
Mice, Inbred ICR
Nephrotoxicity
Oxidative damage
Oxidative Stress - drug effects
Phosphatidylcholine
Phosphatidylcholines - pharmacology
Real-Time Polymerase Chain Reaction
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Summary: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 (0.1ml, 1.2g/kg) was intra-peritoneally injected into 7-week-old ICR mice twice a week. PC in corn oil (0.1ml, 100mg/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.
ISSN:0940-2993
1618-1433
DOI:10.1016/j.etp.2016.08.005