Long-Term Methylglyoxal Treatment Causes Endothelial Dysfunction of Rat Isolated Mesenteric Artery
-
- MUKOHDA Masashi
- Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Aomori 034–8628, Japan
-
- MORITA Tomoka
- Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Aomori 034–8628, Japan
-
- OKADA Muneyoshi
- Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Aomori 034–8628, Japan
-
- HARA Yukio
- Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Aomori 034–8628, Japan
-
- YAMAWAKI Hideyuki
- Laboratory of Veterinary Pharmacology, School of Veterinary Medicine, Kitasato University, Aomori 034–8628, Japan
この論文をさがす
抄録
Methylglyoxal (MGO) is a metabolite of glucose and likely related to pathogenesis of diabetes-related vascular complications including hypertension. In this study, long-term effects of MGO on endothelial function were examined. Rat isolated mesenteric artery was treated for 3 days with MGO using an organ culture method. The contractility, morphology and protein expression of organ-cultured artery were examined. MGO (42 μM, 3 days) impaired acetylcholine (ACh: 1 nM–300 μM)-induced endothelium-dependent relaxation, while it had no effect on sodium nitroprusside (0.1 nM–10 μM)-induced endothelium-independent relaxation. MGO decreased ACh (3 μM)-induced nitric oxide (NO) production as measured by a fluorescence NO indicator, diaminofluorescein-2. Consistently, MGO inhibited ACh (3 μM)-induced phosphorylation of vasodilator stimulated phosphoprotein (an indicator of cyclic GMP production). MGO induced apoptosis in endothelium as detected by TdT-mediated dUTP-biotin nick-end labeling staining. MGO induced accumulation of superoxide in endothelium as detected by dihydroethidium staining. MGO decreased protein expression of endothelial NO synthase (eNOS). Gp91ds-tat (0.1 μM), an inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX), prevented the impairment of endothelium-dependent relaxation and the decrease in eNOS protein caused by MGO. The present results demonstrated that long-term MGO treatment impairs endothelium-dependent relaxation through NOX-derived increased superoxide-mediated endothelial apoptosis.
収録刊行物
-
- The Journal of Veterinary Medical Science
-
The Journal of Veterinary Medical Science 75 (2), 151-157, 2013
公益社団法人 日本獣医学会
- Tweet
キーワード
詳細情報 詳細情報について
-
- CRID
- 1390282681407168384
-
- NII論文ID
- 130001879669
-
- NII書誌ID
- AA10796138
-
- COI
- 1:STN:280:DC%2BC3s%2FgslymtA%3D%3D
-
- ISSN
- 13477439
- 09167250
-
- NDL書誌ID
- 024302761
-
- PubMed
- 23018793
-
- 本文言語コード
- en
-
- データソース種別
-
- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
-
- 抄録ライセンスフラグ
- 使用不可