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在糖尿病小鼠中使用Empagliflozin评估细胞膜血液动力学功能

Kengo Kidokoro¹, David Z I Cherney², Andrea Bozovic³

¹Department of Nephrology and Hypertension, Kawasaki Medical School, Kurashiki, Okayama, Japan (K.K., H.N., M.S., E.K., T.S., N.K.).

|February 19, 2019

概括

在糖尿病小鼠中,像empagliflozin这样的糖共传递剂2抑制剂可降低过. 这种作用由腺和A1腺受体介导,有助于保护.

科学领域:

肝脏病学
药理学
心血管医学

背景情况:

通过减轻过,糖携带体2 (SGLT2) 抑制剂可以保护脏并降低心血管风险.
对SGLT2抑制的反应背后的机制需要进一步阐明.
这项研究研究了empagliflozin对脏的保护作用,重点是血液动力学和管球体反.

研究的目的:

探索SGLT2抑制对的保护作用.
研究质血动力学和管状质反对empagliflozin的影响.
阐明参与调解这些反应的特定分子途径.

主要方法:

使用自发糖尿病Ins2^{+/ Akita}小鼠和C57BL/6对照.
给药的empagliflozin和特定的抑制剂 (神经元氧化合成酶,循环氧化酶-2,A1腺受体对抗剂).
使用体内多光子显微镜和定量尿路生物标志物测量单膜透率 (snGFR).

主要成果:

在糖尿病小鼠中,empagliflozin显著降低过率 (snGFR从15. 8降低到8. 0nL/ min).
在糖尿病小鼠中观察到的empagliflozin改善了 afferent动脉扩张和增加了质蛋白透性.
治疗empagliflozin时观察到尿液内腺分泌量增加,而A1腺受体对抗作用阻断了empagliflozin的功能.

结论:

在SGLT2抑制过程中,腺/ A1腺受体通路对于sngGFR的管球体反调节至关重要.
这些发现突出了SGLT2抑制剂对和心血管有益的关键机制.
恩帕格利弗洛辛通过腺通路介导的关联动脉收缩来减少过.

关键词:

氨酸这种反,生理血液动力学糖转运剂 2 抑制剂

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