Peroxisome Proliferator-Activated Receptor-γ Activators Monascin and Rosiglitazone Attenuate Carboxymethyllysine-Induced Fibrosis in Hepatic Stellate Cells through Regulating the Oxidative Stress Pathway but Independent of the Receptor for Advanced Glycation End Products Signaling

2013 ◽  
Vol 61 (28) ◽  
pp. 6873-6879 ◽  
Author(s):  
Wei-Hsuan Hsu ◽  
Bao-Hong Lee ◽  
Ya-Wen Hsu ◽  
Tzu-Ming Pan
Keyword(s):  
Oxidative Stress ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Peroxisome Proliferator ◽  
Advanced Glycation ◽  
Peroxisome Proliferator Activated Receptor ◽  
Oxidative Stress Pathway ◽  
Glycation End Products ◽  
End Products ◽  
Stress Pathway

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.

Advanced glycation end products enhance the proliferation and activation of hepatic stellate cells

2008 ◽  
Vol 43 (4) ◽  
pp. 298-304 ◽  
Author(s):  
Keiko Iwamoto ◽  
Keishi Kanno ◽  
Hideyuki Hyogo ◽  
Sho-Ichi Yamagishi ◽  
Masayoshi Takeuchi ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products
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