scholarly journals Advanced Glycation End Product (AGE)-AGE Receptor (RAGE) System Upregulated Connexin43 Expression in Rat Cardiomyocytes via PKC and Erk MAPK Pathways

2013 ◽  
Vol 14 (2) ◽  
pp. 2242-2257 ◽  
Author(s):  
Lu Yu ◽  
Yanbo Zhao ◽  
Shengjie Xu ◽  
Fang Ding ◽  
Chongying Jin ◽  
...  
Keyword(s):  
Advanced Glycation ◽  
Rat Cardiomyocytes ◽  
Advanced Glycation End Product ◽  
Erk Mapk ◽  
Mapk Pathways

scholarly journals Autophagy Plays a Protective Role in Advanced Glycation End Product-Induced Apoptosis in Cardiomyocytes

2015 ◽  
Vol 37 (2) ◽  
pp. 697-706 ◽  
Author(s):  
Pengfei Hu ◽  
Hui Zhou ◽  
Ming Lu ◽  
Liping Dou ◽  
Gang Bo ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Treated Group ◽  
Protective Role ◽  
Signalling Pathways ◽  
Control Group ◽  
Advanced Glycation ◽  
Rat Cardiomyocytes ◽  
Advanced Glycation End Product ◽  
Mapk Signalling ◽  
Induced Apoptosis

Background/Aims: To investigate the effect of advanced glycation endproduct-induced autophagy in rat cardiomyocytes and to identify the role of autophagy in advanced glycation end product-induced cell apoptosis. Methods: After cultured rat cardiomyocytes were treated with advanced glycation end products (AGEs), protein expression was detected by western blotting, autophagosomes were observed by electron microscopy, the cell apoptotic rate was determined by flow cytometry, and cell variability was quantified by the MTT assay. Results: After cultured cardiomyocytes were treated with AGEs, the level of autophagy-associated protein LC3-II was up-regulated and SQSTM1/p62 was down-regulated; the number of autophagosomes was increased. Compared with the control group, the apoptotic rate of cardiomyocytes increased, and the cardiomyocyte viability was decreased in the AGE-treated group. Furthermore, pretreating cells with3-MA, an autophagy inhibitor, could enhance these effects. Treatment with AGEs activated phospho-ERK, phospho-JNK, and phospho-p38/MAPK but inhibited phospho-Akt and phospho-mTOR. Pretreatment with an ERK inhibitor and an Akt activator could inhibit AGE-induced autophagy, demonstrating that AGEs induce autophagy in cardiomyocytes through the ERK and Akt signalling pathways. Conclusion: AGEs can induce autophagy through the PI3K/AKT/mTOR and ERK signalling pathways and induce apoptosis through the PI3K/AKT/mTOR and p38/MAPK signalling pathways in rat cardiomyocytes. Autophagy plays a protective role in AGE-induced apoptosis in cardiomyocytes.

Advanced glycation end product-induced activation of NF-kappaB is suppressed by alpha-lipoic acid in cultured endothelial cells

Diabetes ◽  
1997 ◽  
Vol 46 (9) ◽  
pp. 1481-1490 ◽  
Author(s):  
A. Bierhaus ◽  
S. Chevion ◽  
M. Chevion ◽  
M. Hofmann ◽  
P. Quehenberger ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid ◽  
Advanced Glycation ◽  
Advanced Glycation End Product ◽  
Cultured Endothelial Cells ◽  
Nf Kappab

scholarly journals Advanced glycation end product levels were correlated with inflammation and carotid atherosclerosis in type 2 diabetes patients

2020 ◽  
Vol 15 (1) ◽  
pp. 364-372 ◽  
Author(s):  
Jie Li ◽  
Haiyan Shangguan ◽  
Xiaoqian Chen ◽  
Xiao Ye ◽  
Bin Zhong ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Color Doppler ◽  
Enzyme Linked Immunosorbent Assay ◽  
Advanced Glycation ◽  
Advanced Glycation End Product ◽  
Inflammatory Status ◽  
Tnf Α ◽  
Ifn Γ

AbstractDiabetes mellitus with atherosclerosis (AS) adds to the social burden. This study aimed to investigate whether advanced glycation end product (AGE) levels were correlated with inflammation and carotid AS (CAS) in type 2 diabetes mellitus (T2DM) patients. A total of 50 elderly T2DM patients and 50 age-matched senior healthy subjects were recruited in this study. T2DM patients were classified into two groups based on the intima–media thickness (IMT) of the carotid artery from color Doppler ultrasonography. Patients with IMT > 1 mm were classified into the T2DM + CAS group (n = 28), and patients with IMT < 1 mm were assigned as the T2DM + non-atherosclerosis (NAS) group (n = 22). The plasma levels of AGEs, receptor for AGE (RAGE), tumor necrosis factor alpha (TNF-α), and interferon gamma (IFN-γ) of all subjects were measured by enzyme-linked immunosorbent assay. The T-lymphocyte subsets were analyzed by a flow detector. T2DM + CAS patients showed significantly higher concentrations of AGEs, RAGE, TNF-α, and IFN-γ in the peripheral blood. The highest levels of CD4+ T cells were observed in the T2DM + CAS group. The AGE level was positively correlated with the concentrations of RAGE, TNF-α, IFN-γ, and CD4+. In summary, the results showed that the levels of AGEs may be correlated with the inflammatory status in T2DM patients with CAS.

Phytochemicals against anti‐diabetic complications: targeting the advanced glycation end product signaling pathway

2021 ◽  
Vol 44 (4) ◽  
pp. 378-401
Author(s):  
Amna Parveen ◽  
Razia Sultana ◽  
Seung Min Lee ◽  
Tae Hun Kim ◽  
Sun Yeou Kim
Keyword(s):  
Signaling Pathway ◽  
Diabetic Complications ◽  
Advanced Glycation ◽  
Advanced Glycation End Product
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