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首页> 外文期刊>Journal of nephrology. >Na+/Ca2+ exchange inhibitor, KB-R7943, attenuates contrast-induced acute kidney injury
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Na+/Ca2+ exchange inhibitor, KB-R7943, attenuates contrast-induced acute kidney injury

机译：Na + / Ca2 +交换抑制剂KB-R7943可减轻对比剂诱发的急性肾损伤

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Background: Intracellular Ca2+ overload is considered to be a key factor in contrast-induced acute kidney injury (CI-AKI). The Na+/Ca2+ exchanger (NCX) system is one of the main pathways of intracellular Ca2+ overload. We investigated the effects of KB-R7943, an inhibitor of the reverse mode of NCX, on CI-AKI in a rat model. Method: Rats were divided into control group, CI-AKI group and pretreatment groups (with KB-R7943 dose of 5 or 10 mg/kg). CI-AKI was induced by diatrizoate administration in rats with cholesterol-supplemented diet for 8 weeks. Renal function and renal hemodynamics were determined 1 day following contrast medium administration. Renal histopathology was observed by light microscope. Renal tubular apoptosis was examined by TUNEL. Renal endothelin-1 (ET-1) was measured by radioimmunoassay. Renal malondialdehyde (MDA) and catalase (CAT) were measured as oxidative markers. Results: Levels of serum creatinine (Scr), renal ET-1, MDA and CAT, and resistance index (RI) of renal blood vessels increased significantly in CI-AKI rats. The increases in Scr and RI of renal blood vessels induced by diatrizoate were suppressed significantly and dose-dependently by pretreatment with KB-R7943. Histopathological and TUNEL results showed that the contrast medium-induced severe renal tubular necrosis and apoptosis were significantly and dosedependently attenuated by KB-R7943. KB-R7943 significantly suppressed the increment of renal ET-1 content and MDA and CAT level induced by contrast medium administration. Conclusion: Activation of the reverse mode of NCX, followed by ET-1 overproduction and increased oxidative stress, seems to play an important role in the pathogenesis of CI-AKI. The inhibitor of the reverse mode of NCX, KB-R7943, has renoprotective effects on CI-AKI.
机译：背景：细胞内Ca2 +超负荷被认为是造影剂诱发的急性肾损伤（CI-AKI）的关键因素。 Na + / Ca2 +交换器（NCX）系统是细胞内Ca2 +超负荷的主要途径之一。我们在大鼠模型中研究了NCX反向模式抑制剂KB-R7943对CI-AKI的影响。方法：将大鼠分为对照组，CI-AKI组和预处理组（KB-R7943剂量为5或10 mg / kg）。在补充胆固醇的大鼠中，连续8周通过添加泛氮酸盐诱导了CI-AKI。造影剂给药后1天测定肾功能和肾血流动力学。光学显微镜观察肾组织病理。 TUNEL检查肾小管凋亡。肾素-1（ET-1）通过放射免疫测定法进行测量。肾脏丙二醛（MDA）和过氧化氢酶（CAT）被测量为氧化标记。结果：CI-AKI大鼠的血清肌酐（Scr），肾ET-1，MDA和CAT水平以及肾血管抵抗指数（RI）显着增加。通过用KB-R7943预处理，显着地抑制了由泛影酸盐诱导的肾血管Scr和RI的增加，且剂量依赖性。组织病理学和TUNEL结果显示，KB-R7943显着且剂量依赖性地减轻了造影剂引起的严重肾小管坏死和细胞凋亡。 KB-R7943显着抑制了造影剂给药引起的肾ET-1含量和MDA和CAT水平的增加。结论：激活NCX的反向模式，然后产生ET-1过量和增加氧化应激，似乎在CI-AKI的发病机理中起重要作用。 NCX反向模式的抑制剂KB-R7943对CI-AKI具有肾脏保护作用。

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