Advanced Glycation End Products Inhibit the Expression of Collagens Type I and III by Human Gingival Fibroblasts

2009 ◽  
Vol 80 (7) ◽  
pp. 1166-1173 ◽  
Author(s):  
Lei Ren ◽  
Yun Fu ◽  
Yuquan Deng ◽  
Liuying Qi ◽  
Lijian Jin
Keyword(s):  
Advanced Glycation End Products ◽  
Human Gingival Fibroblasts ◽  
Type I ◽  
Gingival Fibroblasts ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals 6-Shogaol Inhibits Advanced Glycation End-Products-Induced IL-6 and ICAM-1 Expression by Regulating Oxidative Responses in Human Gingival Fibroblasts

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3705 ◽  
Author(s):  
Nonaka ◽  
Bando ◽  
Sakamoto ◽  
Inagaki ◽  
Naruishi ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Inflammatory Responses ◽  
Human Gingival Fibroblasts ◽  
Heme Oxygenase 1 ◽  
Gingival Fibroblasts ◽  
Advanced Glycation ◽  
Periodontal Tissues ◽  
Glycation End Products ◽  
End Products ◽  
Oxidative Responses

Advanced glycation end-products (AGEs) cause diabetes mellitus (DM) complications and accumulate more highly in periodontal tissues of patients with periodontitis and DM. AGEs aggravate periodontitis with DM by increasing the expression of inflammation-related factors in periodontal tissues. 6-Shogaol, a major compound in ginger, has anti-inflammatory and anti-oxidative activities. However, the influence of shogaol on DM-associated periodontitis is not well known. In this study, the effects of 6-shogaol on AGEs-induced oxidative and anti-oxidative responses, and IL-6 and ICAM-1 expression in human gingival fibroblasts (HGFs) were investigated. When HGFs were cultured with 6-shogaol and AGEs, the activities of reactive oxygen species (ROS) and antioxidant enzymes (heme oxygenase-1 [HO-1] and NAD(P)H quinone dehydrogenase 1 [NQO1]), and IL-6 and ICAM-1 expressions were investigated. RAGE expression and phosphorylation of MAPKs and NF-κB were examined by western blotting. 6-Shogaol significantly inhibited AGEs-induced ROS activity, and increased HO-1 and NQO1 levels compared with the AGEs-treated cells. The AGEs-stimulated expression levels of receptor of AGE (RAGE), IL-6 and ICAM-1 and the phosphorylation of p38, ERK and p65 were attenuated by 6-shogaol. These results suggested that 6-shogaol inhibits AGEs-induced inflammatory responses by regulating oxidative and anti-oxidative activities and may have protective effects on periodontitis with DM.

scholarly journals Receptor for advanced glycation end-products (RAGE) is an indicator of direct lung injury in models of experimental lung injury

2009 ◽  
Vol 297 (1) ◽  
pp. L1-L5 ◽  
Author(s):  
Xiao Su ◽  
Mark R. Looney ◽  
Naveen Gupta ◽  
Michael A. Matthay
Keyword(s):  
Lung Injury ◽  
Advanced Glycation End Products ◽  
Cell Injury ◽  
Alveolar Epithelial Cell ◽  
Experimental Models ◽  
Alveolar Type ◽  
Type I ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Receptor for advanced glycation end-products (RAGE) is a marker of alveolar type I cells and is elevated in the pulmonary edema fluid of patients with acute lung injury (ALI). We tested the hypothesis that RAGE in the bronchoalveolar lavage (BAL) would be elevated in experimental models of direct ALI characterized by alveolar epithelial cell injury. We developed ELISA measurements for RAGE and studied ALI (direct and indirect) mouse models and collected BAL at specified endpoints to measure RAGE. We also tested whether levels of BAL RAGE correlated 1) with the severity of lung injury in acid and hyperoxia-induced ALI and 2) with the beneficial effect of a novel treatment, mesenchymal stem cells (MSC), in LPS-induced ALI. In ALI models of direct lung injury induced by intratracheal instillation of acid, LPS, or Escherichia coli, the BAL RAGE was 58-, 22-, and 13-fold elevated, respectively. In contrast, BAL RAGE was not detectable in indirect models of ALI induced by an intraperitoneal injection of thiourea or by an intravenous injection of MHC I monoclonal antibody that produces a mouse model of transfusion-related ALI. BAL RAGE did correlate with the severity of lung injury in acid and hyperoxia-induced ALI. In addition, with LPS-induced ALI, BAL RAGE was markedly reduced with MSC treatment. In summary, BAL RAGE is an indicator of ALI, and it may be useful in distinguishing direct from indirect models of ALI as well as assessing the response to specific therapies.

In VitroGlycoxidation of Insoluble Fibrous Type I Collagen: Solubilization and Advanced Glycation End Products

2003 ◽  
Vol 22 (6) ◽  
pp. 527-531 ◽  
Author(s):  
M. Meli ◽  
R. Granouillet ◽  
E. Reynaud ◽  
A. Chamson ◽  
J. Frey ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Type I Collagen ◽  
Type I ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Advanced glycation end products are eliminated by scavenger-receptor-mediated endocytosis in hepatic sinusoidal Kupffer and endothelial cells

1997 ◽  
Vol 322 (2) ◽  
pp. 567-573 ◽  
Author(s):  
Bård SMEDSRØD ◽  
Jukka MELKKO ◽  
Norie ARAKI ◽  
Hiroyuki SANO ◽  
Seikoh HORIUCHI
Keyword(s):  
Advanced Glycation End Products ◽  
Kupffer Cells ◽  
Scavenger Receptor ◽  
Type I ◽  
Advanced Glycation ◽  
Liver Uptake ◽  
Glycation End Products ◽  
End Products

Long-term incubation of proteins with glucose leads to the formation of advanced glycation end products (AGE). Physiological aspects of the catabolism of non-enzymically glycated proteins were studied in vivo and in vitro. AGE-modified BSA (AGE-BSA) was a mixture of high-Mr (cross-linked), monomeric and low-Mr (fragmented) AGE-BSA. After intravenous administration in rat, all three fractions of AGE-BSA accumulated extremely rapidly and almost exclusively in liver. Uptake in liver endothelial, Kupffer and parenchymal cells accounted for approx. 60%, 25% and 10–15% respectively of hepatic elimination. Both cross-linked and monomeric AGE-BSA were efficiently taken up and degraded in cultures of purified liver endothelial and Kupffer cells. Endocytosis of AGE-BSA by these cells was inhibited by several ligands for the scavenger receptor. Although 125I-Hb was not endocytosed in vitro, 125I-AGE-Hb was effectively endocytosed by a mechanism that was subject to inhibition by AGE-BSA. Endocytosis of N-terminal propeptide of type I procollagen, a physiological ligand for the scavenger receptor, was effectively inhibited by AGE-Hb and AGE-BSA. We conclude that AGE-modification renders macromolecules susceptible for elimination via the scavenger receptor of both liver endothelial and Kupffer cells.

scholarly journals Receptor for advanced glycation end-products is a marker of type I lung alveolar cells

2004 ◽  
Vol 9 (2) ◽  
pp. 165-174 ◽  
Author(s):  
Madoka Shirasawa ◽  
Naoyuki Fujiwara ◽  
Susumu Hirabayashi ◽  
Hideki Ohno ◽  
Junko Iida ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Type I ◽  
Advanced Glycation ◽  
Alveolar Cells ◽  
Glycation End Products ◽  
End Products
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