Advanced glycation end products, diabetes and ageing

Naß, Norbert; Bartling, Babett; Santos, Anne Navarrete; Scheubel, R.; Börgermann, Jochen; Silber, Rolf-Edgar; Simm, Andreas

doi:10.1007/s00391-007-0484-9

Cited by 135 publications

(115 citation statements)

References 65 publications

Supporting

Mentioning

105

Contrasting

Unclassified

Order By: Relevance

“…These induced phenotypes may be the result of excessive formation of Reactive Oxygen Species (ROS) and D-gal-induced accumulation of AGEs (Song et al, 1999). ROS damage and AGE accumulation are well known causes of aging and diabetes (Osawa and Kato, 2005;Nass et al, 2007). In addition, many autoantibodies associated with diabetes and aging have been detected (Morohoshi et al, 2012;Ziegler and Bonifacio, 2012;Culina et al, 2013).…”

Section: Ajimentioning

confidence: 99%

Production of Cross-Reactive Autoantibody Binding to Bovine Serum Albumin in the D-Galactose-Induced Aging Mouse Model

Park¹

2014

American Journal of Immunology

View full text Add to dashboard Cite

The D-galactose (D-gal)-induced animal model, generated by repeated subcutaneous D-gal injections over approximately 6 weeks, has been frequently used for diabetes and aging research. However, little research has investigated the direct correlation between D-gal and autoantibody formation despite several reports on diabetes-and aging-related autoantibodies. The purpose of this study was to determine whether repetitive injection of D-gal can induce autoantibody production in mice. First, we used Bovine Serum Albumin (BSA) and Advanced Glycation End products (AGE)-BSA as the test antigens. The immunoreactivity of serum samples from mice treated with D-gal for 6 weeks was evaluated using Enzyme-Linked Immunosorbent Assay (ELISA). We found that serum samples of D-gal-treated mice had significantly high antibody titers against both BSA and AGE-BSA. Furthermore, the result showed that aminoguanidine treatment, an AGE inhibitor tended to decrease this immunoreactivity. The results of competitive inhibition ELISA using BSA and AGE-BSA as the competitors suggested that the serum samples from D-gal-treated mice contained antibodies not only against BSA but also specific to AGE-BSA. To assess whether the immunoreactivity against BSA is comparable to that against Mouse Serum Albumin (MSA), we examined the reactivity of D-gal-induced antibodies against MSA. Unexpectedly, D-gal-induced antibodies did not react with MSA. This suggests that the production of antibodies by Dgal is in response to an unknown antigen(s), aside from MSA, in mice and that this unknown antigen(s) may share similar sequences or three-dimensional structures with BSA.

show abstract

Section: Ajimentioning

confidence: 99%

Production of Cross-Reactive Autoantibody Binding to Bovine Serum Albumin in the D-Galactose-Induced Aging Mouse Model

Park¹

2014

American Journal of Immunology

View full text Add to dashboard Cite

show abstract

“…In in vitro systems, melanoidins mixtures have negligible mutagenic effects (Somoza, 2005), while 5-hydroxymethylfurfural (HMF) is considered a potentially carcinogenic to humans and some epidemiological studies have found an association between acrylamide intake and the occurence of tumors the occurrence of tumors (Capuano & Fogliano, 2011). The formation of advanced glycation end products (AGEs) is observed during normal ageing and occurs inside as well as outside of cells (Nass et al, 2007). These compounds, when cross linking with proteins profoundly affect protein functionality and irreversibly modify chemical properties and functions of diverse biological structures (Barbosa et al, 2008), which seems to be implicated in inflammatory processes and diabetic complications, such as nephropathy and vascular disease (Jakus & Rietbrock, 2004;Linden et al, 2008;Mostafa et al, 2007).…”

Section: Biological Activity Of the Maillard Reaction Products (Mrps)mentioning

confidence: 99%

“…AGEs are a heterogeneous group of compounds that arise non-enzymatically by the reaction of reducing sugar and other α-carbonylic compounds with amino groups on proteins, lipids and nucleic acids. Actually, glycation in living organisms have other pathways that are linked to glucose metabolism and lipid peroxidation, whose products are termed Advanced Lipoxidation End Products (ALEs) (Goldberg et al, 2004;Nass et al, 2007). MRPs/AGEs generated in food and biological systems are shown in Figures 2 and 3.…”

mentioning

confidence: 99%

Maillard Reaction Products in Processed Food: Pros and Cons

Bastos¹,

Monaro²,

Siguemoto³

et al. 2012

Food Industrial Processes - Methods and Equipment

View full text Add to dashboard Cite

“…As a result, high‐molecular‐weight protein and fluorescent entities are produced. These products are referred to as advanced glycation end products (AGEs) 3. Studies pointed out that AGEs were closely correlated with the occurrence, progression, and development of diabetic vascular complications 4…”

Section: Introductionmentioning

confidence: 99%

Matrine‐Type Alkaloids Inhibit Advanced Glycation End Products Induced Reactive Oxygen Species‐Mediated Apoptosis of Aortic Endothelial Cells In Vivo and In Vitro by Targeting MKK3 and p38MAPK Signaling

Liu

Zhang

et al. 2017

JAHA

View full text Add to dashboard Cite

BackgroundThe matrine‐type alkaloids are bioactive components extracted from Sophora flavescens, which is used in treatment of diabetes mellitus in traditional Chinese medicine. Advanced glycation end products mediate diabetic vascular complications. This study was aimed to investigate the protective effects and molecular mechanisms of matrine‐type alkaloids on advanced glycation end products–induced reactive oxygen species–mediated endothelial apoptosis.Methods and ResultsRats aorta and cultured rat aortic endothelial cells were exposed to advanced glycation end products. Matrine‐type alkaloids, p38 mitogen‐activated protein kinase (MAPK) inhibitor, and small interference RNAs against p38 MAPK kinases MAPK kinase kinase (MKK)3 and MKK6 were administrated. Intracellular reactive oxygen species production, cell apoptosis, phosphorylation of MKKs/p38 MAPK, and expression levels of heme oxygenase/NADPH quinone oxidoreductase were assessed. The nuclear factor erythroid 2‐related factor 2 nuclear translocation and the binding activity of nuclear factor erythroid 2‐related factor 2 with antioxidant response element were also evaluated. Matrine‐type alkaloids suppressed intracellular reactive oxygen species production and inhibited endothelial cell apoptosis in vivo and in vitro by recovering phosphorylation of MKK3/6 and p38 MAPK, nuclear factor erythroid 2‐related factor 2 nuclear translocation, and antioxidant response element binding activity, as well as the expression levels of heme oxygenase/NADPH quinone oxidoreductase. p38 MAPK inhibitor treatment impaired the effects of matrine‐type alkaloids in vivo and in vitro. MKK3/6 silencing impaired the effects of matrine‐type alkaloids in vitro.ConclusionsMatrine‐type alkaloids exert endothelial protective effects against advanced glycation end products induced reactive oxygen species–mediated apoptosis by targeting MKK3/6 and enhancing their phosphorylation.

show abstract

Advanced glycation end products, diabetes and ageing

Cited by 135 publications

References 65 publications

Production of Cross-Reactive Autoantibody Binding to Bovine Serum Albumin in the D-Galactose-Induced Aging Mouse Model

Production of Cross-Reactive Autoantibody Binding to Bovine Serum Albumin in the D-Galactose-Induced Aging Mouse Model

Maillard Reaction Products in Processed Food: Pros and Cons

Matrine‐Type Alkaloids Inhibit Advanced Glycation End Products Induced Reactive Oxygen Species‐Mediated Apoptosis of Aortic Endothelial Cells In Vivo and In Vitro by Targeting MKK3 and p38MAPK Signaling

Contact Info

Product

Resources

About