Protective effects of andrographolide derivative AL-1 on high glucose-induced oxidative stress in RIN-m cells

2016 ◽  
Vol 22 (4) ◽  
pp. 499-505 ◽  
Author(s):  
Hui Yan ◽  
Yongmei Li ◽  
Yali Yang ◽  
Zaijun Zhang ◽  
Gaoxiao Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
M Cells ◽  
Protective Effects

Protective Effects of Chungkookjang Extract on High Glucose Induced Oxidative Stress in LLC-PK1Cells

2008 ◽  
Vol 13 (2) ◽  
pp. 84-89 ◽  
Author(s):  
Na-Ri Yi ◽  
Kyoung-Chun Seo ◽  
Ji-Myung Choi ◽  
Eun-Ju Cho ◽  
Young-Ok Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Protective Effects

scholarly journals Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Kaifeng Li ◽  
Mengen Zhai ◽  
Liqing Jiang ◽  
Fan Song ◽  
Bin Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Diabetic Cardiomyopathy ◽  
High Glucose ◽  
Therapeutic Potential ◽  
Ros Generation ◽  
Protective Effects ◽  
Collagen Iii

Hyperglycemia-induced oxidative stress and fibrosis play a crucial role in the development of diabetic cardiomyopathy (DCM). Tetrahydrocurcumin (THC), a major bioactive metabolite of natural antioxidant curcumin, is reported to exert even more effective antioxidative and superior antifibrotic properties as well as anti-inflammatory and antidiabetic abilities. This study was designed to investigate the potential protective effects of THC on experimental DCM and its underlying mechanisms, pointing to the role of high glucose-induced oxidative stress and interrelated fibrosis. In STZ-induced diabetic mice, oral administration of THC (120 mg/kg/d) for 12 weeks significantly improved the cardiac function and ameliorated myocardial fibrosis and cardiac hypertrophy, accompanied by reduced reactive oxygen species (ROS) generation. Mechanically, THC administration remarkably increased the expression of the SIRT1 signaling pathway both in vitro and in vivo, further evidenced by decreased downstream molecule Ac-SOD2 and enhanced deacetylated production SOD2, which finally strengthened antioxidative stress capacity proven by repaired activities of SOD and GSH-Px and reduced MDA production. Additionally, THC treatment accomplished its antifibrotic effect by depressing the ROS-induced TGFβ1/Smad3 signaling pathway followed by reduced expression of cardiac fibrotic markers α-SMA, collagen I, and collagen III. Collectively, these finds demonstrated the therapeutic potential of THC treatment to alleviate DCM mainly by attenuating hyperglycemia-induced oxidative stress and fibrosis via activating the SIRT1 pathway.

scholarly journals DIHYDROMYRICETIN ATTENUATES HIGH GLUCOSE-INDUCED CASPASE 3 EXPRESSION, ROS PRODUCTION AND INCREASES AMPK PHOSPHONYLATION IN PC12 CELLS

2019 ◽  
Vol 8 (5) ◽  
Author(s):  
Shuo Wang ◽  
Lin Wang ◽  
Haijian Li ◽  
Shumei Wang ◽  
Zhenzhen Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Caspase 3 ◽  
Cell Damage ◽  
Neural Function ◽  
Ros Production ◽  
Protective Effects ◽  
Beneficial Effects ◽  
Central Nervous System Dysfunction ◽  
Amp Activated Protein Kinase

Dihydromyricetin (DMY) has a protective effect on neural function under central nervous system dysfunction conditions. There is growing interest concerning the beneficial effects of DMY on treating diabetic neuropathy (DN). This study was carried to detect protective effects of DMY on high glucose (HG)-induced cell damage and related mechanisms. The effect of DMY on cell survival was detected by MTT assay. Caspase-3 and phosphorylated AMP-activated protein kinase (AMPK) was evaluated by Western blotting. The effects of DMY and AMPK agonist AICAR on ROS production was determined. Our results showed that DMY treatment protect against HG-induced cell damage. DMY treatment significantly reduced the expression of caspase-3 and phosphorylated AMPK. ROS production was inhibited by DMY or AMPK agonist AICAR treatment. These studies demonstrate that DMY may inhibit ROS production, caspase-3 expression through AMPK pathway. Keywords: dihydromyricetin, caspase, oxidative stress

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