title: Inhibition of NA(+)/H(+) Exchanger 1 Attenuates Renal Dysfunction Induced by Advanced Glycation End Products in Rats.
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.
authors.affiliation: College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China ; Department of Pharmacology, Pharmaceutical College, Central South University, Changsha 410078, China.
authors.forename: Peng
authors.initials: P
authors.lastname: Li
authors.affiliation: Department of Pharmacology, Pharmaceutical College, Central South University, Changsha 410078, China.
authors.forename: Geng-Rong
authors.initials: GR
authors.lastname: Chen
authors.affiliation: The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, School of Medicine, Shandong University, Jinan 250012, China.
authors.forename: Fu
authors.initials: F
authors.lastname: Wang
authors.affiliation: College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China.
authors.forename: Ping
authors.initials: P
authors.lastname: Xu
authors.affiliation: Department of Pharmacology, Pharmaceutical College, Central South University, Changsha 410078, China ; Medical College of San-Quan, Xinxiang Medical University, Xinxiang 453003, China.
authors.forename: Li-Ying
authors.initials: LY
authors.lastname: Liu
authors.affiliation: College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China ; School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang 453003, China.
authors.forename: Ya-Ling
authors.initials: YL
authors.lastname: Yin
authors.affiliation: College of Pharmacy, Xinxiang Medical University, Xinxiang 453003, China ; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital, School of Medicine, Shandong University, Jinan 250012, China.
authors.forename: Shuang-Xi
authors.initials: SX
authors.lastname: Wang
mesh_terms: D000818:Animals; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D017127:Glycation End Products, Advanced / Q000494:pharmacology*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017923:Sodium-Hydrogen Exchangers / Q000378:metabolism*
chemical_list: D017127:Glycation End Products, Advanced; D017923:Sodium-Hydrogen Exchangers; D008315:Malondialdehyde; D007770:L-Lactate Dehydrogenase; D005978:Glutathione