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Alagebrium chloride, a novel advanced glycation end-product cross linkage breaker, inhibits neointimal proliferation in a diabetic rat carotid balloon injury model.

Authors
 Jin-Bae Kim  ;  Byeong-Wook Song  ;  Sungha Park  ;  Ki-Chul Hwang  ;  Bong-Soo Cha  ;  Yangsoo Jang  ;  Hyun-Chul Lee  ;  Moon-Hyoung Lee 
Citation
 KOREAN CIRCULATION JOURNAL, Vol.40(10) : 520-526, 2010 
Journal Title
KOREAN CIRCULATION JOURNAL
ISSN
 1738-5520 
Issue Date
2010
Keywords
Advanced glycation end-products ; Alagebrium ; Neointimal hyperplasia
Abstract
BACKGROUND AND OBJECTIVES: Vascular perturbation induced by advanced glycation end-products (AGEs) leads to progression of atherosclerosis, plaque instability, and vascular inflammation, which results in a higher risk of neointimal proliferation. Here we investigated the inhibitory effect of alagebrium chloride (ALT-711), a breaker of AGE-based cross links, on neointimal proliferation in a carotid artery balloon injury model in diabetic rats induced by streptozotocin (STZ).

MATERIALS AND METHODS: Rat aortic vascular smooth muscle cells (RASMCs) were treated with 1-100 µM of alagebrium added 24 hours before the addition of AGEs. This in vivo study was done using 8-week-old male rats that were injected intraperitoneally with 80 mg/kg STZ. Sixteen weeks later, the diabetic rats were treated with 10 mg/kg alagebrium for 4 weeks, after which carotid artery balloon injury was induced. After 4 weeks, the animals were sacrificed for histological analysis.

RESULTS: Proliferation of RASMCs was significantly inhibited in alagebrium-treated cells. Alagebrium dose-dependently inhibited AGE-mediated formation of reactive oxygen species (ROS), extracellular signal-regulated kinase phosphorylation, and cyclooxygenase-2 expression. The cellular mechanisms of AGE-induced connective tissue and extracellular matrix expression were decreased in the alagebrium-treated group. This in vivo study shows that expression of AGE receptors and neointima hyperplasia are significantly suppressed in balloon-injured rats treated with alagebrium.

CONCLUSION: Alagebrium treatment in diabetic rats significantly inhibits neointimal hyperplasia after carotid balloon injury due to its inhibition of intracellular ROS synthesis, which results in inhibition of RASMCs proliferation
Files in This Item:
T201004099.pdf Download
DOI
10.4070 / kcj.2010.40.10.520
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Jin Bae(김진배)
Park, Sung Ha(박성하) ORCID logo https://orcid.org/0000-0001-5362-478X
Song, Byeong Wook(송병욱)
Lee, Moon-Hyoung(이문형) ORCID logo https://orcid.org/0000-0002-7268-0741
Lee, Hyun Chul(이현철)
Jang, Yang Soo(장양수) ORCID logo https://orcid.org/0000-0002-2169-3112
Cha, Bong Soo(차봉수) ORCID logo https://orcid.org/0000-0003-0542-2854
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/102603
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