scholarly journals 7-O-Galloyl-D-sedoheptulose Is a Novel Therapeutic Agent against Oxidative Stress and Advanced Glycation Endproducts in the Diabetic Kidney

2009 ◽  
Vol 32 (4) ◽  
pp. 657-664 ◽  
Author(s):  
Noriko Yamabe ◽  
Ki Sung Kang ◽  
Chan Hum Park ◽  
Takashi Tanaka ◽  
Takako Yokozawa
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Agent ◽  
Advanced Glycation Endproducts ◽  
Advanced Glycation ◽  
Diabetic Kidney ◽  
Glycation Endproducts ◽  
Novel Therapeutic ◽  
In The Diabetic Kidney

scholarly journals Metaflammation: Tissue-Specific Alterations of the NLRP3 Inflammasome Platform in Metabolic Syndrome

2018 ◽  
Vol 25 (11) ◽  
pp. 1294-1310 ◽  
Author(s):  
Raffaella Mastrocola ◽  
Manuela Aragno ◽  
Giuseppe Alloatti ◽  
Massimo Collino ◽  
Claudia Penna ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Advanced Glycation Endproducts ◽  
Low Grade ◽  
Advanced Glycation ◽  
Added Sugars ◽  
Physiological Ageing ◽  
Glycation Endproducts ◽  
Inflammatory Status ◽  
Age Related

In the last decades, the extension of life expectancy and the increased consumption of foods rich in saturated fats and added sugars have exposed the general population to emerging health problems. The prevalence of metabolic syndrome (MS), composed of a cluster of factors as obesity, dyslipidemia, hyperglycemia, and hypertension, is rapidly increasing in industrialized and developing countries leading to precocious onset of age-related diseases. Indeed, oxidative stress, accumulation of advanced glycation endproducts, and a chronic low-grade inflammation are common features of MS and physiological ageing. In particular, the entire set of MS factors contributes to the development of an inflammatory status named metaflammation, which has been associated with activation of early innate immune response through the assembling of the multiprotein complex inflammasome. The most investigated family of inflammasome platforms is the NOD-like receptor pyridine containing (NLRP) 3, which is activated by several exogenous and endogenous stimuli, leading to the sequential cleavage of caspase-1 and IL-1β, followed by secretion of active IL-1β. We here collect the most recent findings on NLRP3 activation in MS providing evidence of its central role in disease progression and organ dysfunction in target tissues of metaflammation, in particular in cardiovascular, hepatic and renal complications, with a focus on oxidative stress and advanced glycation endproducts. A wide overview of the most promising strategies for the modulation of NLRP3 activation and related metabolic repercussions is also provided, since the finding of specific pharmacological tools is an urgent requirement to reduce the social and economic burden of MS- and elderly-associated diseases.

scholarly journals Advanced glycation endproducts mediate pro-inflammatory actions in human gestational tissues via nuclear factor-κB and extracellular signal-regulated kinase 1/2

2007 ◽  
Vol 193 (2) ◽  
pp. 269-277 ◽  
Author(s):  
Martha Lappas ◽  
Michael Permezel ◽  
Gregory E Rice
Keyword(s):  
Oxidative Stress ◽  
Human Placenta ◽  
Advanced Glycation Endproducts ◽  
Nuclear Factor Κb ◽  
Mitogen Activated Protein Kinase ◽  
Nuclear Factor ◽  
Advanced Glycation ◽  
Glycation Endproducts ◽  
Gestational Tissues

Processes of human labour include increased oxidative stress, formation of inflammatory mediators (e.g. cytokines) and uterotonic phospholipid metabolites (e.g. prostaglandins). In non-gestational tissues, advanced glycation endproducts (AGE) induce the expression of pro-inflammatory molecules through mitogen-activated protein kinase and nuclear factor κB (NF-κB)-dependent pathways. Thus, the aim of this study was to investigate the effects of AGE on 8-isoprostane (a marker of oxidative stress), pro-inflammatory cytokine and prostaglandin release in human gestational tissues, and to define the signalling pathways involved. Human placenta and gestational membranes (amnion and choriodecidua combined; n=5) were incubated in the absence or presence of AGE–BSA (0.25, 0.5, 1 and 2 mg/ml) for 18 h. AGE significantly increased in vitro release of tumour necrosis factor-α, interleukin (IL)-1β, IL-6, IL-8, prostaglandin (PG)E2, PGF2α and 8-isoprostane from human placenta and gestational membranes. This was associated with a concomitant increase in NF-κB p65 activation and ERK 1/2 phosphorylation. AGE-stimulated 8-isoprostane, cytokine and prostaglandin production was significantly suppressed by the ERK 1/2 inhibitor U0126 and the NF-κB inhibitor BAY 11-7082. In conclusion, AGE mediates inflammatory actions in human gestational tissues. Protein kinases and the NF-κB pathway play an essential role in AGE signalling in human gestational tissues.

Metformin reverts the oxidative stress and apoptosis induced by ages (advanced glycation endproducts) on osteoblastic cells

Bone ◽  
2007 ◽  
Vol 41 (6) ◽  
pp. S2-S3
Author(s):  
AD McCarthy ◽  
C Sedlinsky ◽  
AM Cortizo ◽  
L Bruzzone ◽  
V Arnol ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Advanced Glycation Endproducts ◽  
Osteoblastic Cells ◽  
Advanced Glycation ◽  
Glycation Endproducts
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