Dergiler / Gülhane Tıp Dergisi / 2014 / Cilt: 56 - Sayı: 2

Effect of Methylglyoxal on Soluble Receptor For Advanced Glycation End Products (sRAGE) Of Pre-Osteoblast MC3T3E1 Cell Line

Sayfa
93–96
DOI
—
🏛️Bu makalenin bibliyografik verileri ve tam metin bağlantısı DergiPark üzerinden sağlanmıştır.
DergiPark Kaydı ↗
✨

Yapay Zeka Hızlı Bakış & Çıkarımlar

AI Insight
⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

Iron chelating does not change the sRAGE level.

📌 3 Maddede Bu Makale

🎯
Amaç & Hipotez:Methylgyoxal (MG) is reactive dicarbonyl compound was found in high level in blood of diabetic patients.
📊
Temel Bulgular & Veri:This study aimed to investigate the effect of changes intracellularly redox status on sRAGE levels in preosteoblast MC3T3E1 exposed to MG.
💡
Sonuç & Katkı:Iron chelating does not change the sRAGE level.
🔬Tür:Araştırma Makalesi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Abstract

Methylgyoxal (MG) is reactive dicarbonyl compound was found in high level in blood of diabetic patients. Methlyglyoxal was more reactive compared to glucose and have toxic effect through AGEs. Soluble Receptor for Advanced Glycation End Products (sRAGE) act as a scavenger and decoy receptor for AGEs. This study aimed to investigate the effect of changes intracellularly redox status on sRAGE levels in preosteoblast MC3T3E1 exposed to MG. The changes of redox status was obtained by blockade of superoxide dismutase (Diethylthiocarbamoic acid/DETCA), blockade of gluthatione peroxidase (mercapto succinate/MS), and chelating of iron (defferoxamine/DFX). sRAGE levels was evaluated by enzyme linked imunnosorbent assay technique. The levels of sRAGE in MG-exposed group or DETCA-exposed group was significantly increased than that in control group (P < 0.05). The levels of sRAGE in MG+DETCA-exposed group was significantly decrease compared with DETCA-exposed group (P < 0.05). The levels of sRAGE was significantly increased in MS-exposed group or MG+MS-exposed group than that in control group, respectively (P < 0.05). Concluded that the change of redox status by antioxidant blocker or MG exposure would increases sRAGE levels in preosteoblast MC3T3E1 cell line. The modulation of redox state by antioxidant blocker does not affect sRAGE level in the presence of MG. Iron chelating does not change the sRAGE level.

🔖

Bu Makaleye Atıf Yap

AKBAR, I. Z., PERMATASARİ, N., SOEATMADJİ, D. W., KALIM, H., HİDAYAT, M. (2014). Effect of Methylglyoxal on Soluble Receptor For Advanced Glycation End Products (sRAGE) Of Pre-Osteoblast MC3T3E1 Cell Line. Gülhane Tıp Dergisi, Cilt: 56 - Sayı: 2, 93–96. https://ajindex.com/articles/225300

📄 Tam Metin PDF Okuyucu

📄

PDF görüntüleyici hazırlanıyor...

Kaynakça (10)

  1. Schalkwijk CG, Bezu J, van der Schors RC, Uchida K, Stehouwer CDA, van Hinsbergh VWM. Heat-shock protein 27 is major methylgyoxal-modified protein in endothelial cells. FEBS Lett 2011; 580:1565-70.
  2. Oliveira LMA, Lages A, Gomes RA, Neves H, Familia C, Coelho AV, Quintas A. Insulin glycation by methylglyoxal results in native-like aggregation and inhibition of fibril formation. BMC Biochem 2011; 12:41. Yamagishi S, Imaizumi T: Serum levels of soluble form of receptor for advanced glycation end products (sRAGE) may reflect tissue RAGE expression in diabetes. Arterioscler Thromb Vasc Biol 2007; 27:33-4.
  3. Nakamura K, Yamagishi S, Nakamura Y, Takenaka K, Matsui T, Jinnouchi Y, Imaizumi T. Telmisartan inhibits expression of a receptor for advanced glycation end products (RAGE) in angiotensin-II-exposed endothelial cells and decreases serum levels of soluble RAGE in patients with essential hypertension. Microvasc Res 2005, 70:137-41.
  4. Arabi YM, Dehbi M, Rishu AH, Baturcam E, Kahoul SH, Brits RJ, Naidu B, Bouchama A. sRAGE in diabetic and non-diabetic critically ill patients: effects of intensive insulin therapy. Critical Care 2011; 15:203. Soop A, Sunden-Cullberg J, Albert J, Hallstrom L, Treutiger CJ, Sollevi A. Adenosine infusion attenuates soluble RAGE in endotoxin-induced inflammation in human volunteers. Acta Physiol 2009; 197:47-53.
  5. Yonekura H, Yamamoto Y, Sakurai S, Petrova RG, Abedin MJ, Li H, Yasui K, Takeuchi M, Makita Z, Takasawa S, Okamoto H, Watanabe T, Yamamoto H. Novel splice variants of the receptor for advanced glycation end-products expressed in human vascular endothelial cells and pericytes, and their putative roles in diabetes-induced vascular injury. Biochem J 2003; 370:1097-109.
  6. Nishida S, Endo N, Yamagiwa H, Tanizawa T, Takahashi HE. Number of osteoprogenitor cells in human bone marrow markedly decreases after skeletal maturation. J Bone Mineral Metab 1999; 17(3):171-7.
  7. Arjmandi BH, Juma S, Beharka A, Bapna MS, Akhter M, Meydani SN. Vitamin E improves bone quality in the aged but not in young adult male mice. J Nutr Biochem 2002; 13(9):543-9.
  8. Chan W, Wu H. Protective effects of curcumin on methylglyoxal-induced oxidative DNA damage and cell injury in human mononuclear cells. Acta Pharmacol Sinica 2006; 27(9):1192-8.
  9. Bai X, Lu D, Liu A, Zhang Z, Li X, Zou Z, Zeng W, Cheng B, Luo S. Reactive oxygen species stimulates receptor activator of NF-KB ligand expression in osteoblast. J Biol Chem 2005; 280(17):17487-506.
  10. Akbar IZ, Permatasari N, Soeatma