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首页> 外文期刊>Journal of applied toxicology >Alteration of renal excretion pathways in gentamicin‐induced renal injury in rats
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Alteration of renal excretion pathways in gentamicin‐induced renal injury in rats

机译：庆大霉素诱导大鼠肾损伤肾脏排泄途径的改变

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Abstract The kidney plays a major part in the elimination of many drugs and their metabolites, and drug‐induced kidney injury commonly alters either glomerular filtration or tubular transport, or both. However, the renal excretion pathway of drugs has not been fully elucidated at different stages of renal injury. This study aimed to evaluate the alteration of renal excretion pathways in gentamicin (GEN)‐induced renal injury in rats. Results showed that serum cystatin C, creatinine and urea nitrogen levels were greatly increased by the exposure of GEN (100?mg kg –1 ), and creatinine concentration was increased by 39.7% by GEN (50?mg kg –1 ). GEN dose‐dependently upregulated the protein expression of rOCT1, downregulated rOCT2 and rOAT1, but not affected rOAT2. Efflux transporters, rMRP2, rMRP4 and rBCRP expressions were significantly increased by GEN(100), and the rMATE1 level was markedly increased by GEN(50) but decreased by GEN(100). GEN(50) did not alter the urinary excretion of inulin, but increased metformin and furosemide excretion. However, GEN(100) resulted in a significant decrease of the urinary excretion of inulin, metformin and p ‐aminohippurate. In addition, urinary metformin excretions in vivo were significantly decreased by GEN(100), but slightly increased by GEN(50). These results suggested that GEN(50) resulted in the induction of rOCTs‐rMATE1 and rOAT3‐rMRPs pathway, but not changed the glomerular filtration rate, and GEN(100)‐induced acute kidney injury caused the downregulated function of glomerular filtration ‐rOCTs‐rMATE1 and ‐rOAT1‐rMRPs pathway.
机译：摘要肾脏在消除许多药物及其代谢物中发挥了重要作用，药物诱发的肾脏损伤通常改变肾小球过滤或管状转运，或两者。然而，药物的肾脏排泄途径尚未在肾损伤的不同阶段完全阐明。本研究旨在评估庆大霉素（Gen）诱导大鼠肾损伤肾脏排泄途径的改变。结果表明，通过暴露于丙氨酸（100μmg-1），大大增加血清胱抑素C，肌酐和尿素氮水平，肌酐浓度升高39.7％（50Ωmg-1）。 Gen剂量依赖性上调ROCT1，下调ROCT2和ROAT1的蛋白质表达，但未受影响的ROAT2。基因（100）显着增加了流出转运蛋白，RMRP2，RMRP4和RBCRP表达，并通过Gen（50）显着增加了rMate1水平，但通过Gen（100）减少。 Gen（50）没有改变菊粉的尿排泄，而是增加二甲双胍和呋塞米排泄。然而，Gen（100）导致菊粉，二甲双胍和P-aminofippurate的尿排泄的显着降低。此外，Gen（100）的体内尿合二甲双胍排泄显着降低，但略微增加（50）。这些结果表明，Gen（50）导致诱导ROCTS-CRMATE1和ROAT3-RMRPS途径，但未改变肾小球过滤速率，GEN（100）诱导急性肾损伤导致肾小球过滤的下调功能 - RCOCTS- rmate1和-roat1-rmrps路径。

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