POSSIBLE ROLE OF STATIN ON THE OXIDATIVE STRESS INDUCED BY ADVANCED GLYCATION END PRODUCT (AGE) IN VSMC OF DIABETIC VASCULOPATHY

2008 ◽  
Vol 9 (1) ◽  
pp. 198
Author(s):  
S. Yoon ◽  
Y. Yoon ◽  
K. Hwang ◽  
W. Chang ◽  
H. Kwon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Advanced Glycation ◽  
Advanced Glycation End Product ◽  
Diabetic Vasculopathy

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 SP103PROTECTION ROLE OF AUTOPHAGY IN ADVANCED GLYCATION END PRODUCT-INDUCED MESENGIAL CELL INJURY

2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii412-iii412
Author(s):  
Chien-Ling Lee ◽  
Tien-Fong Lu ◽  
Chih Kang Chiang ◽  
Shing Hwa Liu
Keyword(s):  
Cell Injury ◽  
Advanced Glycation ◽  
Advanced Glycation End Product

Role of peroxisome proliferator–activated receptor-gamma activation on visfatin, advanced glycation end products, and renal oxidative stress in obesity-induced type 2 diabetes mellitus

2018 ◽  
Vol 37 (11) ◽  
pp. 1187-1198 ◽  
Author(s):  
A Tabassum ◽  
T Mahboob
Keyword(s):  
Oxidative Stress ◽  
Renal Damage ◽  
Peroxisome Proliferator ◽  
Advanced Glycation ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Glycation End Products ◽  
End Products

The present study focused on the role of peroxisome proliferator–activated receptor-gamma (PPAR-γ) activation on renal oxidative damages, serum visfatin, and advanced glycation end products (AGEs) in high-fat diet (HFD)-induced type 2 diabetes mellitus. Following the institutional animal ethics committee guidelines, Wistar rats were categorized into five groups: group 1: fed on a normal rat diet; group 2: HFD-induced obese rats (HFD for 8 weeks); group 3: HFD-fed rats treated with rosiglitazone (RSG; 3 mg/kg orally for 7 days); group 4: T2DM rats induced by HFD and low dose of streptozotocin (i.p. 35 mg/kg); group 5: T2DM rats treated with RSG (3 mg/kg orally for 7 days). Serum levels of AGEs and visfatin, renal damage, and oxidative stress were analyzed. Results showed that HFD-induced obesity and T2DM caused an elevated blood glucose, serum AGEs, visfatin, insulin, urea, creatinine, and tissue malondialdehyde, whereas a decreased catalase and superoxide dismutase activity were observed. The PPAR-γ activation via agonist restored these changes. Our findings suggest that AGEs and visfatin possess an important role in the progression of renal oxidative stress, which can be reduced by the PPAR-γ agonist that impede deleterious effects of HFD and HFD-induced T2DM on renal damage.

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