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Gamma linolenic acid exerts anti-inflammatory and anti-fibrotic effects in diabetic nephropathy

Authors
 Do-Hee Kim ; Tae-Hyun Yoo ; Shin-Wook Kang ; Seung Hyeok Han ; Jung Tak Park ; Jwa-Kyung Kim ; Seung Jae Kwak ; Bo Young Nam ; Hye Young Kang ; Soon Ha Lee 
Citation
 Yonsei Medical Journal, Vol.53(6) : 1165~1175, 2012 
Journal Title
 Yonsei Medical Journal 
ISSN
 0513-5796 
Issue Date
2012
Abstract
PURPOSE: This study was undertaken to investigate the effects of gamma linolenic acid (GLA) on inflammation and extracellular matrix (ECM) synthesis in mesangial and tubular epithelial cells under diabetic conditions. MATERIALS AND METHODS: Sprague-Dawley rats were intraperitoneally injected with either a diluent [n=16, control (C)] or streptozotocin [n=16, diabetes (DM)], and eight rats each from the control and diabetic groups were treated with evening primrose oil by gavage for three months. Rat mesangial cells and NRK-52E cells were exposed to medium containing 5.6 mM glucose and 30 mM glucose (HG), with or without GLA (10 or 100 μM). Intercellular adhesion molecule-1 (ICAM-1), monocyte chemoattractant protein-1 (MCP-1), and fibronectin (FN) mRNA and protein expression levels were evaluated. RESULTS: Twenty-four-hour urinary albumin excretion was significantly increased in DM compared to C rats, and GLA treatment significantly reduced albuminuria in DM rats. ICAM-1, MCP-1, FN mRNA and protein expression levels were significantly higher in DM than in C kidneys, and these increases were significantly abrogated by GLA treatment. In vitro, GLA significantly inhibited increases in MCP-1 mRNA expression and protein levels under high glucose conditions in HG-stimulated mesangial and tubular epithelial cells (p<0.05, respectively). ICAM-1 and FN expression showed a similar pattern to the expression of MCP-1. CONCLUSION: GLA attenuates not only inflammation by inhibiting enhanced MCP-1 and ICAM-1 expression, but also ECM accumulation in diabetic nephropathy.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/92145
DOI
10.3349/ymj.2012.53.6.1165
Appears in Collections:
1. 연구논문 > 1. College of Medicine > Yonsei Biomedical Research Center
1. 연구논문 > 1. College of Medicine > Dept. of Internal Medicine
Yonsei Authors
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