Oxidative Stress Mediates Protein Kinase C Activation and Advanced Glycation End Product Formation in a Mesangial Cell Model of Diabetes and High Protein Diet

2009 ◽  
Vol 29 (3) ◽  
pp. 171-180 ◽  
Author(s):  
Katherine R. Tuttle ◽  
Robert J. Anderberg ◽  
Sheryl K. Cooney ◽  
Rick L. Meek
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase C ◽  
Mesangial Cell ◽  
Cell Model ◽  
High Protein Diet ◽  
Product Formation ◽  
Advanced Glycation ◽  
Advanced Glycation End Product ◽  
Kinase C ◽  
Protein Kinase C Activation

scholarly journals Diabetic Neuropathy and Oxidative Stress: Therapeutic Perspectives

2013 ◽  
Vol 2013 ◽  
pp. 1-15 ◽  
Author(s):  
Asieh Hosseini ◽  
Mohammad Abdollahi
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Diabetic Neuropathy ◽  
Aldose Reductase ◽  
New Drugs ◽  
Advanced Glycation ◽  
Kinase C ◽  
Hexosamine Pathway ◽  
And Oxidative Stress

Diabetic neuropathy (DN) is a widespread disabling disorder comprising peripheral nerves' damage. DN develops on a background of hyperglycemia and an entangled metabolic imbalance, mainly oxidative stress. The majority of related pathways like polyol, advanced glycation end products, poly-ADP-ribose polymerase, hexosamine, and protein kinase c all originated from initial oxidative stress. To date, no absolute cure for DN has been defined; although some drugs are conventionally used, much more can be found if all pathophysiological links with oxidative stress would be taken into account. In this paper, although current therapies for DN have been reviewed, we have mainly focused on the links between DN and oxidative stress and therapies on the horizon, such as inhibitors of protein kinase C, aldose reductase, and advanced glycation. With reference to oxidative stress and the related pathways, the following new drugs are under study such as taurine, acetyl-L-carnitine, alpha lipoic acid, protein kinase C inhibitor (ruboxistaurin), aldose reductase inhibitors (fidarestat, epalrestat, ranirestat), advanced glycation end product inhibitors (benfotiamine, aspirin, aminoguanidine), the hexosamine pathway inhibitor (benfotiamine), inhibitor of poly ADP-ribose polymerase (nicotinamide), and angiotensin-converting enzyme inhibitor (trandolapril). The development of modern drugs to treat DN is a real challenge and needs intensive long-term comparative trials.

scholarly journals Role of oxidative stress in advanced glycation end product-induced mesangial cell activation

2002 ◽  
Vol 61 (6) ◽  
pp. 2006-2014 ◽  
Author(s):  
Mark A. Lal ◽  
Hjalmar Brismar ◽  
Ann-Christine Eklöf ◽  
Anita Aperia
Keyword(s):  
Oxidative Stress ◽  
Cell Activation ◽  
Mesangial Cell ◽  
Advanced Glycation ◽  
Advanced Glycation End Product

scholarly journals Amino acids injure mesangial cells by advanced glycation end products, oxidative stress, and protein kinase C

2005 ◽  
Vol 67 (3) ◽  
pp. 953-968 ◽  
Author(s):  
Katherine R. Tuttle ◽  
Emily C. Johnson ◽  
Sheryl K. Cooney ◽  
Robert J. Anderberg ◽  
Edward K. Johnson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Amino Acids ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Advanced Glycation End Products ◽  
Mesangial Cells ◽  
Advanced Glycation ◽  
Kinase C ◽  
Glycation End Products ◽  
End Products

Carnosine prevents testicular oxidative stress and advanced glycation end product formation in D-galactose-induced aged rats

Andrologia ◽  
2017 ◽  
Vol 50 (3) ◽  
pp. e12939 ◽  
Author(s):  
A. F. Aydın ◽  
C. Küçükgergin ◽  
J. Çoban ◽  
I. Doğan-Ekici ◽  
S. Doğru-Abbasoğlu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Product Formation ◽  
Aged Rats ◽  
Advanced Glycation ◽  
Advanced Glycation End Product

scholarly journals Diphlorethohydroxycarmalol Attenuates Methylglyoxal-Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Seon-Heui Cha ◽  
Yongha Hwang ◽  
Soo-Jin Heo ◽  
Hee-Sook Jun
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Mrna Expression ◽  
Human Kidney ◽  
Product Formation ◽  
Diabetic Patients ◽  
Kidney Cells ◽  
Advanced Glycation ◽  
Advanced Glycation End Product ◽  
Hek Cells

Diabetic nephropathy is the leading cause of end-stage renal disease in patients with diabetes mellitus. Oxidative stress has been shown to play an important role in pathogeneses of renal damage in diabetic patients. Here, we investigated the protective effect of diphlorethohydroxycarmalol (DPHC), which is a polyphenol isolated from an edible seaweed, Ishige okamurae, on methylglyoxal-induced oxidative stress in HEK cells, a human embryonic kidney cell line. DPHC treatment inhibited methylglyoxal- (MGO-) induced cytotoxicity and ROS production. DPHC activated the Nrf2 transcription factor and increased the mRNA expression of antioxidant and detoxification enzymes, consequently reducing MGO-induced advanced glycation end product formation. In addition, DPHC increased glyoxalase-1 mRNA expression and attenuated MGO-induced advanced glycation end product formation in HEK cells. These results suggest that DPHC possesses a protective activity against MGO-induced cytotoxicity in human kidney cells by preventing oxidative stress and advanced glycation end product formation. Therefore, it could be used as a potential therapeutic agent for the prevention of diabetic nephropathy.

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