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首页> 外文期刊>American Journal of Physiology >Gene knockout of the Na~+-glucose cotrans-porter SGLT2 in a murine model of acute kidney injury induced by ischemia-reperfusion.
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Gene knockout of the Na~+-glucose cotrans-porter SGLT2 in a murine model of acute kidney injury induced by ischemia-reperfusion.

机译：缺血再灌注诱导的急性肾损伤的鼠模型中Na〜乙酰葡萄糖COTRANS-POTRANS SGLT2的基因敲除。

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In the early proximal tubule, Na~+-glucose cotransporter 2 (SGLT2) mediates the bulk of renal glucose reabsorption. Gene deletion in mice (Sglt2~-/-) was used to determine the role of SGLT2 in acute kidney injury induced by bilateral ischemia-reperfusion (IR). In Sglt2~-/- and littermate wild-type mice, plasma creatinine increased similarly on day 1 after IR. This was associated with an equal increase in both genotypes in the urinary kidney injury molecule-1-to-creatinine ratio, a tubular injury marker, and similarly reduced urine osmolality and increased plasma osmolality, indicating impaired urine concentration. In both IR groups, FITC-sinistrin glomerular filtration rate was equally reduced on day 14, and plasma creatinine was similarly and incompletely restored on day 23. In Sglt2~-/- mice subjected to IR, fractional urinary glucose excretion was increased on day I but reduced and associated with normal renal Na~+-glucose cotransporter 1 (Sglt1) mRNA expression on day 23, suggesting temporary SGLT1 suppression. In wild-type mice subjected to IR, renal Sgltl mRNA was likewise normal on day 23, whereas Sglt2 mRNA was reduced by 57%. In both genotypes, IR equally reduced urine osmolality and renal mRNA expression of the Na~+-K~+-2Cl~-cotransporter and renin on day 23, suggesting thick ascending limb dysfunction, and similarly increased renal mRNA expression of markers of injury, inflammation, oxidative stress, and fibrosis (kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, mono-cyte chemoattractant protein-1, transforming growth factor-beta1, NA-DPH oxidase-2, and collagen type 1). This was associated with equal increases in kidney histological damage scores and similar degree of capillary loss in both genotypes. The data indicate that genetic deletion of SGLT2 did not protect the kidneys in the initial injury phase or the subsequent recovery phase in a mouse model of IR-induced acute kidney injury.
机译：在早期的近端小管中，Na〜+ -GlucoseCotroangerporter 2（SGLT2）介导大量肾葡萄糖重吸收。小鼠中的基因缺失（SGLT2〜/ - ）用于确定SGLT2在双侧缺血再灌注（IR）诱导的急性肾损伤中的作用。在SGLT2〜 - / - 和凋落物野生型小鼠中，血浆肌酐在IR后第1天同样增加。这与尿肾损伤分子-1-肌酐比，管状损伤标记物和类似尿液渗透压和增加的血浆渗透压等血浆渗透性和增加的血浆渗透压等两种基因型增加相关。在IR组中，FITC-辛氏体肾小球过滤速率在第14天同等减少，并且在第23天类似地恢复等离子体肌酐。在对IR进行IR的SGLT2〜 - / - 小鼠中，我的第I天尿葡萄糖排泄但减少和与正常肾Na〜+ -Glucose Cotroansporter 1（SGLT1）mRNA表达在第23天，表明临时SGLT1抑制。在经过IR的野生型小鼠中，在第23天同样是正常的肾SGLTL mRNA，而SGLT2 mRNA减少57％。在两种基因型中，IR同等地减少了Na〜+ -K〜+ -2Cl的尿液渗透压和肾mRNA表达，第23天的转化物和肾素，表明厚度升高的肢体功能障碍，并类似地增加了损伤标记标记的肾mRNA表达，炎症，氧化应激和纤维化（肾损伤分子-1，中性粒细胞明胶酶相关的脂素，单细胞趋化蛋白-1，转化生长因子-β1，Na-DPH氧化酶-2和胶原1）。这与肾脏组织学损伤评分的同等增加相关，并且两种基因型中的毛细血管损失程度相似。数据表明，SGLT2的遗传缺失在IR诱导的急性肾损伤的小鼠模型中，SGLT2的遗传缺失在初始损伤期或随后的恢复相中抑制肾脏。

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