JBP485 improves gentamicin-induced acute renal failure by regulating the expression and function of Oat1 and Oat3 in rats

Guo, Xin; Meng, Qiang; Liu, Qi; Wang, Changyuan; Sun, Huijun; Peng, Jinyong; Ma, Xiaochi; Kaku, Taiichi; Liu, Kexin

doi:10.1016/j.taap.2013.04.029

Cited by 42 publications

(29 citation statements)

References 38 publications

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“…Similar results were also observed in a recent study by Guo et al (2013). The mechanisms of these changes were also investigated in this study.…”

Section: Discussionsupporting

confidence: 92%

“…The present study showed that atorvastatin treatment recovered the function and expression of renal Oat3 in gentamicin-treated rats. Results from the previous study demonstrated that the decreased overoxidation of the kidney could reverse the impairment of Oat1 and Oat3 function and expression in gentamicin-induced acute renal failure (Guo et al 2013). It is likely that the antioxidant effect of atorvastatin in reducing oxidative stress could be responsible for the improved renal Oat3 expression and function.…”

Section: Discussionmentioning

confidence: 93%

“…The regulation of Oat3 function has been studied extensively in the last decade. Recently, the downregulation of expression of Oat1 and Oat3 has been reported in rats with gentamicin-induced nephrotoxicity (Guo et al 2013). Reduced renal Oat1 and Oat3 expression and function would contribute significantly to gentamicin-induced acute renal failure.…”

Section: Introductionmentioning

confidence: 98%

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Atorvastatin improves renal organic anion transporter 3 and renal function in gentamicin‐induced nephrotoxicity in rats

Jaikumkao

Pongchaidecha

Chattipakorn

et al. 2016

Experimental Physiology

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New Findings r What is the central question of this study?This study was designed to determine the renoprotective effects of atorvastatin treatment in an experimental model of gentamicin-induced nephrotoxicity through modulating the Nrf2 pathway by decreasing the oxidative stress.r What is the main finding and its importance?Atorvastatin exerts a nephroprotective effect by attenuating oxidative stress, protecting renal function and renal organic anion transporter 3 function from the effects of gentamicin. Atorvastatin might protect the tissues via its antioxidant property and by modulating the antioxidant enzymes through the Nrf2 signalling pathway, which may be the underlying mechanisms of these protective effects.Recent evidence demonstrates that statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors, exert not only lipid-lowering effects but also antioxidant, anti-inflammatory and anti-apoptotic effects. Nephrotoxicity, a serious side-effect of gentamicin, is related to an increase in reactive oxygen species in the kidney. This study was designed to determine the renoprotective effects of atorvastatin treatment in an experimental model of gentamicin-induced nephrotoxicity. Male Sprague-Dawley rats were used. Nephrotocixity was induced by i.p. injection of gentamicin, 100 mg kg K. Jaikumkao and others oxidative stress than atorvastatin post-treatment. These effects helped to preserve renal function and Oat3 function and expression. These results indicate that atorvastatin has a renoprotective effect against gentamicin-induced nephrotoxicity by decreasing overoxidation in the kidney, and might be used in conjunction with gentamicin to protect against renal damage.

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“…Similar results were also observed in a recent study by Guo et al (2013). The mechanisms of these changes were also investigated in this study.…”

Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 98%

See 1 more Smart Citation

Atorvastatin improves renal organic anion transporter 3 and renal function in gentamicin‐induced nephrotoxicity in rats

Jaikumkao

Pongchaidecha

Chattipakorn

et al. 2016

Experimental Physiology

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“…In contrast, our data suggest that Oat1 protein expression is not changed, although levels tend to decrease in the ob/ob and db/db models. This is in contrast to studies that suggest Oat1 and Oat3 are commonly coordinated together by various stressors and exogenous stressors (Jin et al, 2012;Ulu et al, 2012;Guo et al, 2013). However, consistent with our results, similar findings have been reported in experimental models of cholestasis.…”

Section: Tubular Degenerationsupporting

confidence: 85%

Renal Xenobiotic Transporter Expression is Altered in Multiple Experimental Models of Nonalcoholic Steatohepatitis

et al. 2014

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Nonalcoholic fatty liver disease is the most common chronic liver disease, which can progress to nonalcoholic steatohepatitis (NASH). Previous investigations demonstrated alterations in the expression and activity of hepatic drug transporters in NASH. Moreover, studies using rodent models of cholestasis suggest that compensatory changes in kidney transporter expression occur to facilitate renal excretion during states of hepatic stress; however, little information is currently known regarding extrahepatic regulation of drug transporters in NASH. The purpose of the current study was to investigate the possibility of renal drug transporter regulation in NASH across multiple experimental rodent models. Both rat and mouse NASH models were used in this investigation and include: the methionine and choline-deficient (MCD) diet, atherogenic diet, fa/fa rat, ob/ob and db/db mice. Histologic and pathologic evaluations confirmed that the MCD and atherogenic rats as well as the ob/ob and db/db mice all developed NASH. In contrast, the fa/fa rats did not develop NASH but did develop extensive renal injury compared with the other models. Renal mRNA and protein analyses of xenobiotic transporters suggest that compensatory changes occur in NASH to favor increased xenobiotic secretion. Specifically, both apical efflux and basolateral uptake transporters are induced, whereas apical uptake transporter expression is repressed. These results suggest that NASH may alter the expression and potentially function of renal drug transporters, thereby impacting drug elimination mechanisms in the kidney.

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“…Peptide transporters (PEPTs) not only serve to mediate the absorption of nutrients but also function in the transport of exogenous compounds, such as dipeptide and tripeptide, as well as a variety of peptidomimetic agents (Bai and Amidon, 1992;Cang et al, 2010;Guo et al, 2012aGuo et al, , 2012bGuo et al, , 2013. The stably transfected HeLa-hPEPT1 cell is a very specific in vitro model that helps to better screen, predict and understand the routes of transport across the intestinal membranes via PEPT1.…”

Section: Introductionmentioning

confidence: 99%

Simultaneous determination of three dipeptides (JBP485, Gly–Sar and JBP923) in the cell lysates by liquid chromatography‐tandem mass spectrometry: application to identify the function of the PEPT1 transfected cell

Guo

Meng

Liu

et al. 2014

Biomedical Chromatography

Self Cite

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A simple and rapid liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for the simultaneous determination of JBP485, Gly-Sar and JBP923 in the cell lysates using methanol as a deproteinization solvent was developed and validated. Detection was performed by turbo ionspray ionization in multiple reaction monitoring mode using the transitions of m/z 147.1 → m/z 90.1 for Gly-Sar, m/z 201.1 → m/z 86.1 for JBP485, m/z 219.1 → m/z 86.1 for JBP923 and m/z 152.0 → m/z 110.0 for paracetamol (internal standard). The analytes were separated on a Hypersil ODS C18 HPLC column using isocratic elution mode with a mobile phase containing 0.1% formic acid in water-methanol (97:3, v/v) at a flow rate of 0.2 mL/min. The calibration curves were demonstrated to be linear over the concentration range of 5.00-5000 nm with coefficient of 0.9968 for Gly-Sar, 0.9975 for JBP485 and 0.9952 for JBP923. The intra- and inter-day precisions were <10.2% for each quality contro; level, and the accuracy was within ±5.6% for each analyte. The matrix effect, the extraction recovery and stabilities of LC-MS/MS analysis were also investigated. This validated method was successfully applied to the simultaneous determination of JBP485, Gly-Sar and JBP923 in the cell lysates for identification of stably transfected HeLa cells with human PEPT1.

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JBP485 improves gentamicin-induced acute renal failure by regulating the expression and function of Oat1 and Oat3 in rats

Cited by 42 publications

References 38 publications

Atorvastatin improves renal organic anion transporter 3 and renal function in gentamicin‐induced nephrotoxicity in rats

Atorvastatin improves renal organic anion transporter 3 and renal function in gentamicin‐induced nephrotoxicity in rats

Renal Xenobiotic Transporter Expression is Altered in Multiple Experimental Models of Nonalcoholic Steatohepatitis

Simultaneous determination of three dipeptides (JBP485, Gly–Sar and JBP923) in the cell lysates by liquid chromatography‐tandem mass spectrometry: application to identify the function of the PEPT1 transfected cell

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