Strawberry fruit ( Fragaria x ananassa cv. Romina) extenuates iron‐induced cardiac oxidative injury via effects on redox balance, angiotensin‐converting enzyme, purinergic activities, and metabolic pathways

2020 ◽  
Vol 44 (8) ◽  
Author(s):  
Ochuko L. Erukainure ◽  
Veronica F. Salau ◽  
Ayodeji B. Oyenihi ◽  
Ndumiso Mshicileli ◽  
Md. Shahidul Islam
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Metabolic Pathways ◽  
Oxidative Injury ◽  
Redox Balance ◽  
Fragaria X Ananassa ◽  
Converting Enzyme ◽  
Strawberry Fruit

Interspecies comparison of the metabolic pathways of perindopril, a new angiotensin-converting enzyme (ACE) inhibitor

Xenobiotica ◽  
1990 ◽  
Vol 20 (8) ◽  
pp. 787-800 ◽  
Author(s):  
L. Grislain ◽  
M. T. Mocquard ◽  
J. F. Dabe ◽  
M. Bertrand ◽  
W. Luijten ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Metabolic Pathways ◽  
Ace Inhibitor ◽  
Converting Enzyme ◽  
Interspecies Comparison

scholarly journals Alamandine attenuates hepatic fibrosis by regulating autophagy induced by NOX4-dependent ROS

2020 ◽  
Vol 134 (7) ◽  
pp. 853-869
Author(s):  
Yun Huang ◽  
Yang Li ◽  
Anni Lou ◽  
Guo zhen Wang ◽  
Ye Hu ◽  
...  
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Hepatic Fibrosis ◽  
Collagen Synthesis ◽  
Renin Angiotensin System ◽  
Redox Balance ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Protein Levels

Abstract Angiotensin II (Ang II) has been reported to aggravate hepatic fibrosis by inducing NADPH oxidase (NOX)-dependent oxidative stress. Alamandine (ALA) protects against fibrosis by counteracting Ang II via the MAS-related G-protein coupled (MrgD) receptor, though the effects of alamandine on hepatic fibrosis remain unknown. Autophagy activated by reactive oxygen species (ROS) is a novel mechanism of hepatic fibrosis. However, whether autophagy is involved in the regulation of Ang II-induced hepatic fibrosis still requires investigation. We explored the effect of alamandine on hepatic fibrosis via regulation of autophagy by redox balance modulation. In vivo, alamandine reduced CCl4-induced hepatic fibrosis, hydrogen peroxide (H2O2) content, protein levels of NOX4 and autophagy impairment. In vitro, Ang II treatment elevated NOX4 protein expression and ROS production along with up-regulation of the angiotensin converting enzyme (ACE)/Ang II/Ang II type 1 receptor (AT1R) axis. These changes resulted in the accumulation of impaired autophagosomes in hepatic stellate cells (HSCs). Treatment with NOX4 inhibitor VAS2870, ROS scavenger N-acetylcysteine (NAC), and NOX4 small interfering RNA (siRNA) inhibited Ang II-induced autophagy and collagen synthesis. Alamandine shifted the balance of renin–angiotensin system (RAS) toward the angiotensin converting enzyme 2 (ACE2)/alamandine/MrgD axis, and inhibited both Ang II-induced ROS and autophagy activation, leading to attenuation of HSCs migration or collagen synthesis. In summary, alamandine attenuated liver fibrosis by regulating autophagy induced by NOX4-dependent ROS.

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