Related Experiment Video
Updated: Mar 28, 2026

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
Published on: May 10, 2024
Inhibition of NA(+)/H(+) Exchanger 1 Attenuates Renal Dysfunction Induced by Advanced Glycation End Products in Rats
Peng Li1, Geng-Rong Chen2, Fu Wang3
1College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China ; Department of Pharmacology, Pharmaceutical College, Central South University, Changsha 410078, China.
Abstract:
It has been recognized that sodium hydrogen exchanger 1 (NHE1) is involved in the development of diabetic nephropathy. The role of NHE1 in kidney dysfunction induced by advanced glycation end products (AGEs) remains unknown. Renal damage was induced by AGEs via tail vein injections in rats. Function and morphology of kidney were determined. Compared to vehicle- or BSA-treated rats, AGEs caused abnormalities of kidney structures and functions in rats, accompanied with higher MDA level and lower GSH content. Gene expressions of NHE1 gene and TGF-β1 in the renal cortex and urine were also increased in AGEs-injected rats. Importantly, all these detrimental effects induced by AGEs were reversed by inhibition of NHE1 or suppression of oxidative stress. These pieces of data demonstrated that AGEs may activate NHE1 to induce renal damage, which is related to TGF-β1.
Related Concept Videos
Heart Failure Drugs: Inhibitors of Renin-Angiotensin System
Antihypertensive Drugs: Direct Renin Inhibitors
Antihypertensive Drugs: Action of Diuretics
Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors
Dipeptidyl Peptidase 4 Inhibitors

