Effects of candesartan cilexetil and amlodipine orotate on receptor for advanced glycation end products expression in the aortic wall of Otsuka Long-Evans Tokushima Fatty (OETFF) type 2 diabetic rats

The receptor for advanced glycation end products (RAGE) plays a key role in the development of vascular inflammation and acceleration of atherosclerosis in type 2 diabetes. We investigated the effect of candesartan cilexetil (CDRT) and amlodipine orotate (AMDP) on the expression of RAGE in the aorti...

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Published inArchives of pharmacal research Vol. 39; no. 4; pp. 565 - 576
Main Authors Kang, Min-Kyu, Chung, Woo-Baek, Hong, Seul-Ki, Kim, Ok-Ran, Ihm, Sang-Hyun, Chang, Kiyuk, Seung, Ki-Bae
Format Journal Article
LanguageEnglish
Published Seoul Pharmaceutical Society of Korea 01.04.2016
대한약학회
Subjects
Amlodipine - pharmacology
Amlodipine - therapeutic use
Animals
Aorta - drug effects
Aorta - enzymology
Aorta - metabolism
Benzimidazoles - pharmacology
Benzimidazoles - therapeutic use
Biphenyl Compounds - pharmacology
Biphenyl Compounds - therapeutic use
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - metabolism
Diabetic Angiopathies - metabolism
Diabetic Angiopathies - prevention & control
Humans
MAP Kinase Signaling System - drug effects
Medicine
Pharmacology/Toxicology
Pharmacy
Rats, Inbred Strains
Receptor for Advanced Glycation End Products - antagonists & inhibitors
Research Article
Tetrazoles - pharmacology
Tetrazoles - therapeutic use
약학
Advanced glycation end products
Receptor for advanced glycation end products
Diabetes mellitus
Calcium channel blockers
Angiotensin receptor blockers
Online AccessGet full text

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Abstract The receptor for advanced glycation end products (RAGE) plays a key role in the development of vascular inflammation and acceleration of atherosclerosis in type 2 diabetes. We investigated the effect of candesartan cilexetil (CDRT) and amlodipine orotate (AMDP) on the expression of RAGE in the aortic walls of Otsuka Long-Evans Tokushima Fatty (OLETF) rats and AGE-treated endothelial cells. Twenty five-week-old OLETF rats were randomized to 8 week treatments consisting of CDRT (n = 8), AMDP (n = 8) or saline (control, n = 8). Immunohistochemical and dihydroethidine staining revealed reduced RAGE and reactive oxygen species (ROS) signals in rats treated with CDRT or AMDP compared with control rats. Both CDRT and AMDP suppressed the expression of p22phox and p47phox NADPH oxidase subunits. However, only CDRT significantly reduced expression of phosphorylated extracellular signal regulated kinase (pERK)1/2 in the aortic wall of OLETF rats. In addition, both drugs reduced RAGE expression and total and mitochondrial ROS production in the AGE-treated endothelial cells. Both ARBs and CCBs reduced RAGE expression in the aortic walls of OLETF rats, which was attributed to decreased ROS production through inhibition of NADPH oxidase. In addition, only CDRT reduced aortic expression of RAGE via suppression of the ERK1/2 pathway unlike AMDP.
AbstractList The receptor for advanced glycation end products (RAGE) plays a key role in the development of vascular inflammation and acceleration of atherosclerosis in type 2 diabetes. We investigated the effect of candesartan cilexetil (CDRT) and amlodipine orotate (AMDP) on the expression of RAGE in the aortic walls of Otsuka Long-Evans Tokushima Fatty (OLETF) rats and AGE-treated endothelial cells. Twenty five-week-old OLETF rats were randomized to 8 week treatments consisting of CDRT (n = 8), AMDP (n = 8) or saline (control, n = 8). Immunohistochemical and dihydroethidine staining revealed reduced RAGE and reactive oxygen species (ROS) signals in rats treated with CDRT or AMDP compared with control rats. Both CDRT and AMDP suppressed the expression of p22phox and p47phox NADPH oxidase subunits. However, only CDRT significantly reduced expression of phosphorylated extracellular signal regulated kinase (pERK)1/2 in the aortic wall of OLETF rats. In addition, both drugs reduced RAGE expression and total and mitochondrial ROS production in the AGE-treated endothelial cells. Both ARBs and CCBs reduced RAGE expression in the aortic walls of OLETF rats, which was attributed to decreased ROS production through inhibition of NADPH oxidase. In addition, only CDRT reduced aortic expression of RAGE via suppression of the ERK1/2 pathway unlike AMDP.
The receptor for advanced glycation endproducts (RAGE) plays a key role in the development ofvascular inflammation and acceleration of atherosclerosisin type 2 diabetes. We investigated the effect of candesartancilexetil (CDRT) and amlodipine orotate (AMDP)on the expression of RAGE in the aortic walls of OtsukaLong-Evans Tokushima Fatty (OLETF) rats and AGEtreatedendothelial cells. Twenty five-week-old OLETFrats were randomized to 8 week treatments consisting ofCDRT (n = 8), AMDP (n = 8) or saline (control, n = 8). Immunohistochemical and dihydroethidine stainingrevealed reduced RAGE and reactive oxygen species(ROS) signals in rats treated with CDRT or AMDP comparedwith control rats. Both CDRT and AMDP suppressedthe expression of p22phox and p47phox NADPH oxidasesubunits. However, only CDRT significantly reducedexpression of phosphorylated extracellular signal regulatedkinase (pERK)1/2 in the aortic wall of OLETF rats. Inaddition, both drugs reduced RAGE expression and totaland mitochondrial ROS production in the AGE-treatedendothelial cells. Both ARBs and CCBs reduced RAGEexpression in the aortic walls of OLETF rats, which wasattributed to decreased ROS production through inhibitionof NADPH oxidase. In addition, only CDRT reduced aorticexpression of RAGE via suppression of the ERK1/2 pathwayunlike AMDP. KCI Citation Count: 6
Author Chang, Kiyuk
Chung, Woo-Baek
Kang, Min-Kyu
Hong, Seul-Ki
Seung, Ki-Bae
Ihm, Sang-Hyun
Kim, Ok-Ran
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  givenname: Seul-Ki
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  organization: Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea
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  surname: Kim
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  givenname: Sang-Hyun
  surname: Ihm
  fullname: Ihm, Sang-Hyun
  email: heartihmsh@yahoo.co.kr
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– sequence: 6
  givenname: Kiyuk
  surname: Chang
  fullname: Chang, Kiyuk
  organization: Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea
– sequence: 7
  givenname: Ki-Bae
  surname: Seung
  fullname: Seung, Ki-Bae
  organization: Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea
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Keywords Advanced glycation end products
Receptor for advanced glycation end products
Diabetes mellitus
Calcium channel blockers
Angiotensin receptor blockers
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Snippet The receptor for advanced glycation end products (RAGE) plays a key role in the development of vascular inflammation and acceleration of atherosclerosis in...
The receptor for advanced glycation endproducts (RAGE) plays a key role in the development ofvascular inflammation and acceleration of atherosclerosisin type 2...
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SubjectTerms Amlodipine - pharmacology
Amlodipine - therapeutic use
Animals
Aorta - drug effects
Aorta - enzymology
Aorta - metabolism
Benzimidazoles - pharmacology
Benzimidazoles - therapeutic use
Biphenyl Compounds - pharmacology
Biphenyl Compounds - therapeutic use
Diabetes Mellitus, Experimental - complications
Diabetes Mellitus, Experimental - metabolism
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - metabolism
Diabetic Angiopathies - metabolism
Diabetic Angiopathies - prevention & control
Humans
MAP Kinase Signaling System - drug effects
Medicine
Pharmacology/Toxicology
Pharmacy
Rats, Inbred Strains
Receptor for Advanced Glycation End Products - antagonists & inhibitors
Research Article
Tetrazoles - pharmacology
Tetrazoles - therapeutic use
약학
Title Effects of candesartan cilexetil and amlodipine orotate on receptor for advanced glycation end products expression in the aortic wall of Otsuka Long-Evans Tokushima Fatty (OETFF) type 2 diabetic rats
URI https://link.springer.com/article/10.1007/s12272-016-0728-6
https://www.ncbi.nlm.nih.gov/pubmed/26960737
https://search.proquest.com/docview/1781541373
https://www.kci.go.kr/kciportal/ci/sereArticleSearch/ciSereArtiView.kci?sereArticleSearchBean.artiId=ART002100098
Volume 39
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