??-amyloid peptide potentiates inflammatory responses induced by lipopolysaccharide, interferon-gamma and "advanced glycation endproducts" in a mouse microglia cell line

2002 ◽  
Vol 2002 (Fall) ◽  
Author(s):  
Jovana Gasic-Milenkovic ◽  
Sladjana Dukic-Stefanovic ◽  
Winnie Deuther-Conrad ◽  
Gerald M??nch
Author(s):  
Annayara C. F. Fernandes ◽  
Jeane B. Melo ◽  
Vanize M. Genova ◽  
Ádina L. Santana ◽  
Gabriela Macedo

Background: Glycation is a chemical reaction that synthesize advanced glycation endproducts (AGEs). The AGEs irreversibly damage macromolecules present in tissues and organs, leading to the impairment of biological functions. For instance, the accumulation of AGEs induces oxidative stress and consequently inflammatory responses in human body, leading to the on set/worsening of diseases, including obesity, asthma, cognitive impairment, and cancer. There is a current demand on natural and low-cost sources of antiglycant agents. As a result, food phytochemicals presented promising results to inhibit glycation and consequently, the formation of AGEs. Objective: Here, we describe the mechanism of glycation on the worsening of diseases, the methods os detection, and the current findings on the use of phytochemicals (phenolic compounds, phytosterols, carotenoids, terpenes and vitamins) as natural therapeuticals to inhibit health damages via inhibition of AGEs in vitro and in vivo. Methods: This manuscript reviewed publications available in the PubMed and Science Direct databases dated from the last 20 years on the uses of phytochemicals to inhibit the AGEs in vitro and in vivo. Also, recent patents on the use of anti-glycant drugs were reviewed using the Google Advanced Patents database. Results and Discussion: Phenolic compounds have been mostly studied to inhibit AGEs. Food phytochemicals derived from agroindustry wastes, including peanut skins, and the bagasses derived from citrus and grapes are promising antiglycant agents via scavenging of free radicals, metal ions, the suppression of metabolic pathways that induces inflammation, the activation of pathways that promote antioxidant defense, the blocking of AGE connection with the receptor for advanced glycation endproducts (RAGE). Conclusion: Phytochemicals derived from agroindustry are promising anti-glycants, which can be included to replace synthetic drugs for AGE inhibition, and consequently to act as a therapeutical strategy to prevent and treat diseases caused by AGEs, including diabetes, ovarian cancer, osteoporosis, and Alzheimer’s disease.


FEBS Letters ◽  
1997 ◽  
Vol 410 (2-3) ◽  
pp. 481-484 ◽  
Author(s):  
Andreas Simm ◽  
Gerald Münch ◽  
Farshid Seif ◽  
Oliver Schenk ◽  
August Heidland ◽  
...  

Author(s):  
Shi Fang Yan ◽  
Ravichandran Ramasamy ◽  
Ann Marie Schmidt

Recent and compelling investigation has expanded our view of the biological settings in which the products of nonenzymatic glycation and oxidation of proteins and lipids – the advanced glycation endproducts (AGEs) – form and accumulate. Beyond diabetes, natural ageing and renal failure, AGEs form in inflammation, oxidative stress and in ischaemia–reperfusion. The chief signal transduction receptor for AGEs – the receptor for AGEs (RAGE) – is a multiligand-binding member of the immunoglobulin superfamily. In addition to AGEs, RAGE binds certain members of the S100/calgranulin family, high-mobility group box 1 (HMGB1), and β-amyloid peptide and β-sheet fibrils. Recent studies demonstrate beneficial effects of RAGE antagonism and genetic deletion in rodent models of atherosclerosis and ischaemia–reperfusion injury in the heart and great vessels. Experimental evidence is accruing that RAGE ligand generation and release during ischaemia–reperfusion may signal through RAGE, thus suggesting that antagonism of this receptor might provide a novel form of therapeutic intervention in heart disease. However, it is plausible that innate, tissue-regenerative roles for these RAGE ligands may also impact the failing heart – perhaps through RAGE and/or distinct receptors. In this review, we focus on RAGE and the consequences of its activation in the cardiovasculature.


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