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.

scholarly journals Dehydroepiandrosterone Administration Counteracts Oxidative Imbalance and Advanced Glycation End Product Formation in Type 2 Diabetic Patients

Diabetes Care ◽  
2007 ◽  
Vol 30 (11) ◽  
pp. 2922-2927 ◽  
Author(s):  
E. Brignardello ◽  
C. Runzo ◽  
M. Aragno ◽  
M. G. Catalano ◽  
M. Cassader ◽  
...  
Keyword(s):  
Product Formation ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Type 2 Diabetic Patients ◽  
Advanced Glycation End Product ◽  
Type 2 Diabetic

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 Advanced Glycation end Products, Oxidative Stress and Diabetic Nephropathy

2010 ◽  
Vol 3 (2) ◽  
pp. 101-108 ◽  
Author(s):  
Sho-ichi Yamagishi ◽  
Takanori Matsui
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Stress Generation ◽  
Stress System ◽  
Diabetic Patients ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Stage Renal Disease

About 246 million people worldwide had diabetes in 2007. The global figure of people with diabetes is projected to increase to 370 million in 2030. As the prevalence of diabetes has risen to epidemic proportions worldwide, diabetic nephropathy has become one of the most challenging health problems. Therapeutic options such as strict blood glucose and blood pressure controls are effective for preventing diabetic nephropathy, but are far from satisfactory, and the number of diabetic patients on end-stage renal disease is still increasing. Therefore, a novel therapeutic strategy that could halt the progression of diabetic nephropathy should be developed. There is accumulating evidence that advanced glycation end products (AGEs), senescent macroprotein derivatives formed at an accelerated rate under diabetes, play a role in diabetic nephropathy via oxidative stress generation. In this paper, we review the pathophysiological role of AGEs and their receptor (RAGE)-oxidative stress system in diabetic nephropathy.

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