The renal protective effects of nitrite salts in diabetic nephropathy model rats.

一氧化氮（NO）在多种生理过程中发挥着多能性作用。NO是由NO合成酶（NOS）产生的，NOS的紊乱与糖尿病肾病有关。因此，人们认为亚硝酸盐通过非酶还原或酶还原产生一氧化氮是其具有保护肾功能的原因。然而，在本研究中，我们发现亚硝酸盐抑制细胞内ATP水平，然后激活5 ' amp激活的蛋白激酶（AMPK），并随后激活内皮NOS。内皮细胞AMPK-eNOS通路的激活在亚硝酸盐的作用中起到了重要的肾保护作用，除了亚硝酸盐产生一氧化氮不依赖于一氧化氮。

Nitric oxide (NO) plays multipotent effects in many kinds of physiological processes. NO is generated by NO synthase (NOS), and disorders in the NOS is known to be related to diabetic nephropathy. Therefore, it has been believed that the production of NO from nitrite by non-enzymatic or enzymatic reduction responsible for the renoprotective effects of it. However, in this study, we found that nitrite suppress intracellular ATP level, then activates 5’AMP-activated protein kinase(AMPK), and following endotherial NOS activation. The activation of AMPK-eNOS pathway in endotherial cells is supposed to play a significant renal protective role in the nitrite action in addition to the NOS-independent NO production by nitrite.