Kefir peptide (Kef-1) as an emerging approach for the treatment of oxidative stress and inflammation in 2K1C mice

2022 ◽  
Author(s):  
Rafaela Aires ◽  
Fernanda Gobbi Amorim ◽  
Larissa Zambom Côco ◽  
Amanda Pompermayer da Conceição ◽  
Tadeu Ériton Caliman Zanardo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
Bioactive Molecules ◽  
Converting Enzyme ◽  
The Rich ◽  
Potential Use

The benefits of Kefir consumption are due, in part, to the rich composition of bioactive molecules released from fermentation. Angiotensin-converting enzyme (ACE) inhibitors are bioactive molecules with potential use in...

scholarly journals A clinical dose of angiotensin-converting enzyme (ACE) inhibitor and heterozygous ACE deletion exacerbate Alzheimer's disease pathology in mice

2019 ◽  
Vol 294 (25) ◽  
pp. 9760-9770 ◽  
Author(s):  
Shuyu Liu ◽  
Fujiko Ando ◽  
Yu Fujita ◽  
Junjun Liu ◽  
Tomoji Maeda ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Angiotensin Converting Enzyme ◽  
Amyloid Precursor Protein ◽  
Ace Inhibitors ◽  
Ace Inhibitor ◽  
Precursor Protein ◽  
Causative Role ◽  
Converting Enzyme ◽  
Clinical Dose

Inhibition of angiotensin-converting enzyme (ACE) is a strategy used worldwide for managing hypertension. In addition to converting angiotensin I to angiotensin II, ACE also converts neurotoxic β-amyloid protein 42 (Aβ42) to Aβ40. Because of its neurotoxicity, Aβ42 is believed to play a causative role in the development of Alzheimer's disease (AD), whereas Aβ40 has neuroprotective effects against Aβ42 aggregation and also against metal-induced oxidative damage. Whether ACE inhibition enhances Aβ42 aggregation or impairs human cognitive ability are very important issues for preventing AD onset and for optimal hypertension management. In an 8-year longitudinal study, we found here that the mean intelligence quotient of male, but not female, hypertensive patients taking ACE inhibitors declined more rapidly than that of others taking no ACE inhibitors. Moreover, the sera of all AD patients exhibited a decrease in Aβ42-to-Aβ40–converting activity compared with sera from age-matched healthy individuals. Using human amyloid precursor protein transgenic mice, we found that a clinical dose of an ACE inhibitor was sufficient to increase brain amyloid deposition. We also generated human amyloid precursor protein/ACE+/− mice and found that a decrease in ACE levels promoted Aβ42 deposition and increased the number of apoptotic neurons. These results suggest that inhibition of ACE activity is a risk factor for impaired human cognition and for triggering AD onset.

scholarly journals ACE2 Nascence, trafficking, and SARS-CoV-2 pathogenesis: the saga continues

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Sally Badawi ◽  
Bassam R. Ali
Keyword(s):  
Cell Surface ◽  
Angiotensin Converting Enzyme ◽  
The Novel ◽  
Converting Enzyme ◽  
Post Translational Modifications ◽  
Angiotensin Converting Enzyme 2 ◽  
Viral Attachment ◽  
Novel Coronavirus ◽  
Effective Medication ◽  
Potential Use

AbstractWith the emergence of the novel coronavirus SARS-CoV-2 since December 2019, more than 65 million cases have been reported worldwide. This virus has shown high infectivity and severe symptoms in some cases, leading to over 1.5 million deaths globally. Despite the collaborative and concerted research efforts that have been made, no effective medication for COVID-19 (coronavirus disease-2019) is currently available. SARS-CoV-2 uses the angiotensin-converting enzyme 2 (ACE2) as an initial mediator for viral attachment and host cell invasion. ACE2 is widely distributed in the human tissues including the cell surface of lung cells which represent the primary site of the infection. Inhibiting or reducing cell surface availability of ACE2 represents a promising therapy for tackling COVID-19. In this context, most ACE2–based therapeutic strategies have aimed to tackle the virus through the use of angiotensin-converting enzyme (ACE) inhibitors or neutralizing the virus by exogenous administration of ACE2, which does not directly aim to reduce its membrane availability. However, through this review, we present a different perspective focusing on the subcellular localization and trafficking of ACE2. Membrane targeting of ACE2, and shedding and cellular trafficking pathways including the internalization are not well elucidated in literature. Therefore, we hereby present an overview of the fate of newly synthesized ACE2, its post translational modifications, and what is known of its trafficking pathways. In addition, we highlight the possibility that some of the identified ACE2 missense variants might affect its trafficking efficiency and localization and hence may explain some of the observed variable severity of SARS-CoV-2 infections. Moreover, an extensive understanding of these processes is necessarily required to evaluate the potential use of ACE2 as a credible therapeutic target.

scholarly journals Inhibition of Central Angiotensin Converting Enzyme Exerts Anxiolytic Effects by Decreasing Brain Oxidative Stress

2011 ◽  
Vol 30 (2) ◽  
pp. 109-114 ◽  
Author(s):  
Alin Ciobica ◽  
Lucian Hritcu ◽  
Veronica Nastasa ◽  
Manuela Padurariu ◽  
Walther Bild
Keyword(s):  
Oxidative Stress ◽  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Elevated Plus Maze ◽  
Enzyme Inhibitor ◽  
Lipid Peroxidation Product ◽  
Converting Enzyme ◽  
Plus Maze ◽  
Antioxidant Defense Enzymes ◽  
Brain Oxidative Stress

Inhibition of Central Angiotensin Converting Enzyme Exerts Anxiolytic Effects by Decreasing Brain Oxidative StressThis study investigated the effects of angiotensin II and captopril intracerebroventricular administration on anxiety status and brain oxidative stress. Elevated plus maze was used in order to asses the anxiety-like behavior, while the biochemical analysis included the determination of some antioxidant defense enzymes like superoxide dismutase and glutathione peroxidase and also a lipid peroxidation product (malondialdehyde). Our results provide additional evidence of angiotensin II induced anxiety-like effects and increased prooxidant status. Moreover, the blockade of angiotensin II, by the administration of an angiotensin converting enzyme inhibitor (captopril) resulted in anxiolytic effects and decreased oxidative stress status. In addition, we found a significant correlation between the time spent by rats in the open arms of the elevated plus maze and oxidative stress markers. This could raise important therapeutic issues regarding the anxiolytic effects of some angiotensin converting enzyme inhibitors used primarily for hypertension, such as captopril. Also, it seems that oxidative stress could play an important part in these actions.

scholarly journals Normal-phase thin-layer chromatography of some angiotensin converting enzyme (ACE) inhibitors and their metabolites

2009 ◽  
Vol 74 (6) ◽  
pp. 677-688 ◽  
Author(s):  
Jadranka Odovic ◽  
Mirjana Aleksic ◽  
Biljana Stojimirovic ◽  
Dusanka Milojkovic-Opsenica ◽  
Zivoslav Tesic
Keyword(s):  
Angiotensin Converting Enzyme ◽  
Thin Layer ◽  
Thin Layer Chromatography ◽  
Ace Inhibitors ◽  
Reversed Phase ◽  
Normal Phase ◽  
Converting Enzyme ◽  
Reversed Phase Chromatography ◽  
Aqueous Solvent ◽  
Layer Chromatography

The separation and chromatographic behaviour of five ACE (angiotensin converting enzyme) inhibitors and their four active metabolites were investigated by normal-phase thin-layer chromatography on silica using several mono- and binary non-aqueous solvent systems. The linear relationship between the RM values and the composition of employed mobile phase was obtained. The hydrophobicity parameters 0M R and C0 were determined from the regression data of the plots, analogous to reversed-phase chromatography. The chromatographically obtained hydrophobicity parameters were correlated with the calculated log P values. The current results were correlated with the lipophilicity of the studied ACE inhibitors and their metabolites, previously estimated by reversed-phase chromatography.

scholarly journals The effect of angiotensin-converting enzyme inhibitors on clinical outcomes in patients with ischemic cardiomyopathy and midrange ejection fraction: a post hoc subgroup analysis from the PEACE trial

2018 ◽  
Vol 12 (12) ◽  
pp. 351-359 ◽  
Author(s):  
Talal Alzahrani ◽  
John Tiu ◽  
Gurusher Panjrath ◽  
Allen Solomon
Keyword(s):  
Ejection Fraction ◽  
Angiotensin Converting Enzyme ◽  
Clinical Outcomes ◽  
Ace Inhibitors ◽  
Subgroup Analysis ◽  
Ischemic Cardiomyopathy ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
All Cause Mortality ◽  
Post Hoc

Background: There have been significant advances in the treatment of patients with cardiomyopathy with reduced ejection fraction (EF < 40%). However, there is a dearth of information in the treatment of patients with cardiomyopathy and midrange EF (40–50%). Current guidelines state to treat these patients similarly to patients with cardiomyopathy and preserved EF. Data from the Prevention of Events with Angiotensin-Converting Enzyme Inhibition (PEACE) trial were used to elucidate whether angiotensin-converting enzyme (ACE) inhibitors improve clinical outcomes in patients with ischemic cardiomyopathy and midrange EF. Methods: A post hoc subgroup analysis of the PEACE trial was conducted to evaluate the effect of ACE inhibitors in a subgroup of patients with ischemic cardiomyopathy and midrange EF (40–50%). A Chi-square test and a Student‘s t-test were used to examine and compare the binary and continuous variables of baseline characteristics and outcomes between experimental and comparison groups. Results: We studied a subgroup of patients from the PEACE trial with ischemic cardiomyopathy and midrange EF ( n = 2512 of 8290 total patients). Patients were assigned to either the interventional group ( n = 1247) or the placebo group ( n = 1265). There were no significant differences in baseline demographic and health characteristics between the two groups. During a total of 7 years (mean 4.7 years) of follow up, the risk of composite outcomes [all-cause mortality, nonfatal myocardial infarction, and stroke; relative risk (RR) 0.79, 95% confidence interval (CI) 0.63–0.98; p = 0.03] and all-cause mortality (RR 0.85, 95% CI 0.73–0.99; p = 0.03) was reduced in patients treated with trandolapril. Conclusion: This study revealed the benefit of ACE inhibitors among patients with ischemic cardiomyopathy and midrange EF.

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