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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Impaired renal organic anion transport 1 (SLC22A6) and its regulation following acute myocardial infarction and reperfusion injury in rats
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Impaired renal organic anion transport 1 (SLC22A6) and its regulation following acute myocardial infarction and reperfusion injury in rats

机译：肾脏有机阴离子输送1（SLC22A6）受损及其调控后大鼠急性心肌梗死和再灌注损伤后

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Acute kidney injury (AKI) is a high frequent and common complication following acute myocardial infarction (AMI). This study examined and identified the effect of AMI-induced AKI on organic anion transporter 1 (Oat1) and Oat3 transport using clinical setting of pre-renal AKI in vivo. Cardiac ischaemia (CI) and cardiac ischaemia and reperfusion (CIR) were induced in rats by 30-min left anterior descending coronary artery occlusion and 30-min occlusion followed by 120-min reperfusion, respectively. Renal hemodynamic parameters, mitochondrial function and Oat1/Oat3 expression and function were determined along with biochemical markers. Results showed that CI markedly reduced renal blood flow and pressure by approximately 40%, while these parameters were recovered during reperfusion. CI and CIR progressively attenuated renal function and induced oxidative stress by increasing plasma BUN, creatinine and malondialdehyde levels. Correspondingly, SOD, GPx, CAT mRNAs were decreased, while TNF alpha, IL1 beta, COX2, iNOS, NOX2, NOX4, and xanthine oxidase were increased. Mitochondrial dysfunction as indicated by increasing ROS, membrane depolarisation, swelling and caspase3 activation were shown. Early significant detection of AKI; KIM1, IL18, was found. All of which deteriorated para-aminohippurate transport by down-regulating Oat1 during sudden ischaemia. This consequent blunted the trafficking rate of Oat1/Oat3 transport via down-regulating PKC zeta/Akt and up-regulating PKC alpha/NF kappa B during CI and CIR. Thus, this promising study indicates that CI and CIR abruptly impaired renal Oat1 and regulatory proteins of Oat1/Oat3, which supports dysregulation of remote sensing and signalling and inter-organ/organismal communication. Oat1, therefore, could potentially worsen AKI and might be a potential therapeutic target for early reversal of such injury.
机译：急性肾损伤（AKI）是急性心肌梗死（AMI）后的高频率和常见并发症。本研究检测并鉴定了在体内预肾炎前肾炎的临床凝视上的AMI诱导的AKI对有机阴离子转运蛋白1（OAT1）和OAT3运输的影响。在大鼠左前期下降冠状动脉闭塞和30分钟后，在大鼠中诱导心脏缺血和心脏缺血和再灌注（CIR）和再灌注（CIR），分别为120分钟再灌注。与生物化学标志物相同测定肾血液动力学参数，线粒体功能和OAT1 / OAT3表达和功能。结果表明，CI显着降低了肾血流和压力约40％，而在再灌注期间回收这些参数。 CI和Cir逐渐减弱肾功能，通过增加血浆面包，肌酐和丙二醛水平来诱导氧化应激。相应地，SOD，GPX，猫MRNA被降低，而TNFα，IL1β，COX2，INOS，NOX2，NOX4和黄嘌呤氧化酶增加。显示了通过增加ROS，膜去偏振，溶胀和Caspase3活化来表示的线粒体功能障碍。早期重大检测AKI;找到了Kim1，IL18。所有这些，在突然的缺血期间，通过下调oat1恶化的副氨基研究。因此，在CI和CIR中，通过下调PKC Zeta / Akt和Up-Chrencate PKCα/ NF Kappa B钝化OAT1 / OAT3运输的贩运率。因此，该有前途的研究表明，CI和CIR突然受损的肾脏OAT1和OAT1 / OAT3的调节蛋白，其支持遥感和信号传导和器官间/有机体通信的失调。因此，OAT1可能会使AKI潜在地恶化，并且可能是早期逆转这种伤害的潜在治疗目标。

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