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ZHANG Rui¹, WANG Min², JANG Xixiu²,HU Qiaoni¹, ZHENG Jifang²

( 1. College of Public Health, Guilin Medical University, Guilin 541001, China; 2. Guangxi KeyLaboratory of Tumor Immunology and Microenvironmental Regulation, Faculty of BasicMedical Sciences, Guilin Medical University, Guilin 541001.China)

Abstract Objeetive 'To investigate whether hydrogen sulfide ( H,S) can alleviate uranium-induced ratsnephrotoxicity by antagonizing carbonyl stress. Methods SD male rats were divided into four groups:normal control group, GYY4137 (H,$ donor) treatment group, uranium exposure group, and GYY4137treatment group. The contents of creatinine and Blood urea nitrogen in urine were determined by microplatemethod and colorimetry. Kidney tissue damage was examined by HE staining. Kidney cell apoptosis wasdeteeted by Tunel method, Thiobarbituric Acid Reactive Substanees(TBARS)and 4-Hydroxynonenal(4-HNE)contents were determined by enzyme-inked immunosorbent assay and MDA content wasdetermined by thio Barbituric acid method. The contents of protein carbonylation ( PCO ) and 8-hydroxyDeoxyguanosine ( 8-0hdG) were measured by spectrophotometry. Western blots was used to detect theexpression of aldehyde metabolic enzymes including alcohol dehydrogenase 1( ADH1 ), aldehydedehydrogenase gene 2(ALDH2),aldo-keto-reductase-7A1( AKR7A1). Results Uranium exposuredecreased the contents of creatinine and Blood urea nitrogen, led to structural damage of renal tissue,induced kidney cells apoptosis, inereased the content of active aldehydes, PCO, 8-0hdG, and reducedthe expression of aldehyde metabolie enzymes. The difference is statistically significant ( P < 0. 05 ).However, GYY4137 administration reversed the above experimental indicators of uranium effeet ( P<0.05). Conclusion H,S$ can induce the expression of aldehyde metabolism enzymes, promote activealdehyde metabolism, and alleviate carbonyl stress,resulting in antagonize uranium-triggered ratsnephrotoxicity.

Keywords:hydrogen sulfide; carbonyl stress; uranium; nephrotoxicity

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