scholarly journals Cardioprotective Effects of Dietary Phytochemicals on Oxidative Stress in Heart Failure by a Sex-Gender-Oriented Point of View

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Klara Komici ◽  
Valeria Conti ◽  
Sergio Davinelli ◽  
Leonardo Bencivenga ◽  
Giuseppe Rengo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Point Of View ◽  
World Population ◽  
Efficacy And Safety ◽  
Innovative Strategy ◽  
Dietary Phytochemicals ◽  
Clinical Models ◽  
Cardioprotective Effects ◽  
Therapeutic Tools

Dietary phytochemicals are considered an innovative strategy that helps to reduce cardiovascular risk factors. Some phytochemicals have been shown to play a beneficial role in lipid metabolism, to improve endothelial function and to modify oxidative stress pathways in experimental and clinical models of cardiovascular impairment. Importantly, investigation on phytochemical effect on cardiac remodeling appears to be promising. Nowadays, drug therapy and implantation of devices have demonstrated to ameliorate survival. Of interest, sex-gender seems to influence the response to HF canonical therapies. In fact, starting by the evidence of the feminization of world population and the scarce efficacy and safety of the traditional drugs in women, the search of alternative therapeutic tools has become mandatory. The aim of this review is to summarize the possible role of dietary phytochemicals in HF therapy and the evidence of a different sex-gender-oriented response.

PPARβ/δ Priming Enhances the Anti-Apoptotic and Therapeutic Properties of Mesenchymal Stromal Cells in Myocardial Ischemia-Reperfusion Injury

2021 ◽  
Author(s):  
Charlotte Sarre ◽  
Rafael Contreras Lopez ◽  
Nitirut Nerpernpisooth ◽  
Christian Barrere ◽  
Sarah Bahraoui ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Mesenchymal Stromal Cells ◽  
Stromal Cells ◽  
Ex Vivo ◽  
Phase Iii ◽  
Therapeutic Properties ◽  
Cardioprotective Effects

Abstract Background: Mesenchymal Stromal Cells (MSC) have been widely used for their therapeutic properties in many clinical applications including myocardial infarction. Despite promising preclinical results and evidences of safety and efficacy in phases I/ II, inconsistencies in phase III trials have been reported. In a previous study, we have shown using MSC derived from the bone marrow of PPARβ/δ (Peroxisome proliferator-activated receptors β/δ) knockout mice that the acute cardioprotective properties of MSC during the first hour of reperfusion are PPARβ/δ-dependent but not related to the anti-inflammatory effect of MSC. However, the role of the modulation of PPARβ/δ expression on MSC cardioprotective and anti-apoptotic properties has never been investigated. Objectives: The aim of this study was to investigate the role of PPARβ/δ modulation (inhibition or activation) in MSC therapeutic properties in vitro and ex vivo in an experimental model of myocardial infarction.Methods and results: Naïve MSC and MSC pharmacologically activated or inhibited for PPARβ/δ were challenged with H202. Through specific DNA fragmentation quantification and qRT-PCR experiments, we evidenced in vitro an increased resistance to oxidative stress in MSC pre-treated by the PPARβ/δ agonist GW0742 versus naïve MSC. In addition, PPARβ/δ-priming allowed to reveal the anti-apoptotic effect of MSC on co-cultured cardiomyocytes. When injected during reperfusion in an ex vivo heart model of myocardial infarction, PPARβ/δ-primed MSC at a dose of 3.75x105 MSC/heart provided the same cardioprotective efficiency than 7.5x105 naïve MSC, identified as the optimal dose in our model. These enhanced short-term cardioprotective effects were associated with an increase in both anti-apoptotic effects and the number of MSC detected in the left ventricular wall at 1 hour of reperfusion. By contrast, inhibition of PPARβ/δ before their administration in post-ischemic hearts during reperfusion decreased their cardioprotective effects. Conclusion: Altogether these results revealed that PPARβ/δ-primed MSC exhibit an increased resistance to oxidative stress and enhanced anti-apoptotic properties on cardiac cells in vitro. PPARβ/δ-priming appears as an innovative strategy to enhance the cardioprotective effects of MSC and to decrease the injected doses. These results could be of major interest to improve MSC efficacy for the cardioprotection of injured myocardium in AMI patients.

The Protective Mechanism of Cannabidiol in Cardiac Injury: A Systematic Review of Non-Clinical Studies

2019 ◽  
Vol 25 (22) ◽  
pp. 2499-2507 ◽  
Author(s):  
Mohammad R.H. Shayesteh ◽  
Hamed Haghi-Aminjan ◽  
Mohammad J. Mousavi ◽  
Saeideh Momtaz ◽  
Mohammad Abdollahi
Keyword(s):  
Oxidative Stress ◽  
Clinical Studies ◽  
Cardiac Injury ◽  
Pleiotropic Effect ◽  
Protective Mechanism ◽  
Search Terms ◽  
Cardioprotective Effects ◽  
Apoptosis And Inflammation ◽  
Meta Analyses

Background: Cardiac disease is accounted as the leading cause of worldwide morbidity and mortality. The disease is characterized by the overproduction of reactive oxygen and/or nitrogen species (ROS/RNS), and induction of oxidative stress. Cannabidiol (CBD) is a non-psychoactive ingredient of marijuana that has been reported to be safe and well tolerated in patients. Due to its pleiotropic effect, CBD has been shown to exert cytoprotective effects. This study intended to clarify the mechanisms and the potential role of CBD regarding cardiac injuries treatment. Methods: A systematic literature search was conducted, according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines, in the electronic databases including PubMed, Web of Science, Scopus, and Embase up to June 2019 using predefined search terms in the titles and abstracts. Accordingly, a set of pre-specified inclusion and exclusion criteria were considered and 8 articles were ultimately included in this study. Results: Our findings demonstrate that CBD has multi-functional protective assets to improve cardiac injuries; preliminary through scavenging of free radicals, and reduction of oxidative stress, apoptosis, and inflammation. Conclusion: CBD can protect against cardiac injuries, mainly through its antioxidative and antiapoptotic effects on the basis of non-clinical studies. The cardioprotective effects of the CBD need to be further studied in welldesigned clinical trials.

Dietary Phytochemicals: As a Natural Source of Antioxidants

2021 ◽  
Author(s):  
Manju Singh Makhaik ◽  
Arvind K. Shakya ◽  
Raosaheb Kale
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Free Radical ◽  
Brain Dysfunction ◽  
Cellular Inflammation ◽  
Hepatic Diseases ◽  
Dietary Phytochemicals ◽  
Free Radical Formation ◽  
Prevention And Cure

Since time immemorial, plants are used as the source of food and medicine. It can be traced back to the start of humanity. Bringing plant-based food, such as fruits, vegetables, and whole grains, rich in phytochemicals, with beneficial nutrients, opens the door for healthy living. The health benefits are partly attributed to the compounds which possess antioxidants. Several epidemiological observations have shown an opposite relationship between consumption of plant-based foods, rich in phytochemicals, and many diseases including cancer. The majority of the ailments are related to oxidative stress induced by free radicals. Free radicals are extremely unstable with a very short half-life, highly reactive molecule which leads to oxidative damage to macromolecules such as proteins, DNA, and lipids. Free radical induced cellular inflammation appears to be a major contributing factor to cause aging, and degenerative diseases such as cancer, cardiovascular diseases, diabetes, hepatic diseases, renal ailments, and brain dysfunction. Free radicals have been caught up in the pathogenesis of several diseases. Providentially, free radical formation is controlled naturally by phytochemicals, through their antioxidant potential which plays a key role in preventing many diseases including cancer by suppressing oxidative stress-induced DNA damage. Keeping these facts in mind, an attempt has been made to highlight the oxidative stress, enzymatic and non-enzymatic antioxidant, dietary phytochemicals and their role of in disease prevention and cure.

A Review on Mitochondrial Dysfunction and Oxidative stress due to Complex-Ⅰ in Parkinson Disease

2021 ◽  
pp. 167-170
Author(s):  
V Nuthan Kumar Babu ◽  
Navneet Khurana
Keyword(s):  
Oxidative Stress ◽  
Parkinson Disease ◽  
Mitochondrial Dysfunction ◽  
Neurodegenerative Disorder ◽  
Dimethyl Fumarate ◽  
World Population ◽  
Emerging Therapies ◽  
And Oxidative Stress ◽  
Transplantation Therapy

Parkinson’s disease (PD) is the common physical movement disorder, and it is 2nd most progressive widespread neurodegenerative disorder all over the world, and it is reported that and essential 10 million, over 0.3 % of the total world population. A thoughtful reduction of the neurotransmitter dopamine (DA) in the striatum is the main cause of these motor symptoms, collectively known as parkinsonism. Mitochondria serves as most important organelle in most of the cells and are essential for life and it is also called as heart for all cellular metabolisms. The main and most important role of mitochondria is generation of ATP via oxidative phosphorylation. In this study will study about how complex Ⅰ deficiency effects the mitochondrial and oxidative stress and reactive oxygen species which cause mitochondrial dysfunction and we also study emerging therapies for Parkinson disease with the help of coenzyme Q10 and some genes like FUN-14, FUNDC-1 and dimethyl fumarate or BG-12 in some phases of clinical trials and also by cell transplantation therapy and in future this study helps in finding how this sporadic Parkinson disease occurs in parkinsonism.

Ghrelin and Cardiovasculature

2010 ◽  
Vol 06 ◽  
pp. 64
Author(s):  
Jörgen Isgaard ◽  
Keyword(s):  
Cardiovascular Disease ◽  
Binding Sites ◽  
Cardiovascular Effects ◽  
Inotropic Effects ◽  
Future Studies ◽  
Gh Secretion ◽  
Cardioprotective Effects ◽  
Therapeutic Tools

Apart from stimulating growth hormone (GH) secretion and a regulatory role for appetite and metabolism, it has become increasingly clear that GH secretagogues (GHS) and ghrelin exert a number of effects on the cardiovascular system. The main cardiovascular actions of GHS are possible inotropic effects, vasodilation, reported cardioprotective effects against ischaemia andin vitroeffects on cardiomyocytes involving cell proliferation and antiapoptotic actions. An interesting and intriguing feature of the cardiovascular effects of GHS is that they may be exerted directly on the heart and vasculature rather than being mediated by GH. Evidence to suggest this is the finding of GHS binding sites on cardiomyocytes and the fact that some of the effects of GHS can be expressed also in the absence of GH. Although these results offer interesting possibilities for ghrelin and/or GHS to be used as therapeutic tools in cardiovascular disease, larger clinical trials in this area are still lacking. Future studies aiming at evaluating a role of GHS and ghrelin in the treatment of cardiovascular disease are warranted.

scholarly journals Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Giovanna Cenini ◽  
Ana Lloret ◽  
Roberta Cascella
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Diseases ◽  
Aging Process ◽  
Molecular Mechanisms ◽  
High Energy ◽  
Point Of View ◽  
Antioxidant Defenses ◽  
Mitochondrial Oxidative Stress ◽  
Cellular Processes

Age is the main risk factor for a number of human diseases, including neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, which increasing numbers of elderly individuals suffer. These pathological conditions are characterized by progressive loss of neuron cells, compromised motor or cognitive functions, and accumulation of abnormally aggregated proteins. Mitochondrial dysfunction is one of the main features of the aging process, particularly in organs requiring a high-energy source such as the heart, muscles, brain, or liver. Neurons rely almost exclusively on the mitochondria, which produce the energy required for most of the cellular processes, including synaptic plasticity and neurotransmitter synthesis. The brain is particularly vulnerable to oxidative stress and damage, because of its high oxygen consumption, low antioxidant defenses, and high content of polyunsaturated fats very prone to be oxidized. Thus, it is not surprising the importance of protecting systems, including antioxidant defenses, to maintain neuronal integrity and survival. Here, we review the role of mitochondrial oxidative stress in the aging process, with a specific focus on neurodegenerative diseases. Understanding the molecular mechanisms involving mitochondria and oxidative stress in the aging and neurodegeneration may help to identify new strategies for improving the health and extending lifespan.

scholarly journals Role of the eNOS Uncoupling and the Nitric Oxide Metabolic Pathway in the Pathogenesis of Autoimmune Rheumatic Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Anna Łuczak ◽  
Marta Madej ◽  
Agata Kasprzyk ◽  
Adrian Doroszko
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Rheumatic Diseases ◽  
Common Mechanism ◽  
World Population ◽  
Autoimmune Rheumatic Diseases ◽  
Enos Uncoupling ◽  
Cardiovascular Morbidity And Mortality

Atherosclerosis and its clinical complications constitute the major healthcare problems of the world population. Due to the central role of endothelium throughout the atherosclerotic disease process, endothelial dysfunction is regarded as a common mechanism for various cardiovascular (CV) disorders. It is well established that patients with rheumatic autoimmune diseases are characterized by significantly increased prevalence of cardiovascular morbidity and mortality compared with the general population. The current European guidelines on cardiovascular disease (CVD) prevention in clinical practice recommend to use a 1,5-factor multiplier for CV risk in rheumatoid arthritis as well as in other autoimmune inflammatory diseases. However, mechanisms of accelerated atherosclerosis in these diseases, especially in the absence of traditional risk factors, still remain unclear. Oxidative stress plays the major role in the endothelial dysfunction and recently is strongly attributed to endothelial NO synthase dysfunction (eNOS uncoupling). Converted to a superoxide-producing enzyme, uncoupled eNOS not only leads to reduction of the nitric oxide (NO) generation but also potentiates the preexisting oxidative stress, which contributes significantly to atherogenesis. However, to date, there are no systemic analyses on the role of eNOS uncoupling in the excess CV mortality linked with autoimmune rheumatic diseases. The current review paper addresses this issue.

scholarly journals Dexmedetomidine Provides Protection to Neurons Against OGD/R-Induced Oxidative Stress and Neuronal Apoptosis

2020 ◽  
Author(s):  
Deming Xu ◽  
Changbi Zhou ◽  
Juanyun Lin ◽  
Wenhui Cai ◽  
Wei Lin
Keyword(s):  
Oxidative Stress ◽  
Neuronal Apoptosis ◽  
Survival Rates ◽  
Glucose Deprivation ◽  
Point Of View ◽  
Dependent Manner ◽  
Oxygen And Glucose Deprivation ◽  
Protein Levels ◽  
Related Proteins

Abstract Background: Dexmedetomidine, a potent α2-adrenoceptor (α2-AR) agonist, is extensively used in the operating room (OR) and intensive care unit (ICU) and has applied in several diseases. However, the precise role of dexmedetomidine in oxygen and glucose deprivation/reoxygenation (OGD/R)-treated neurons, and the mechanisms underlying its effect, has yet to be elucidated. Methods: OGD/R-treated neurons served as a cellular model in our study. Western blotting was used to investigate the protein levels of α-adrenergic receptor (α-AR) in OGD/R-treated neurons, apoptosis related proteins (Bcl-2, Bax and Cleaved Caspase 3) and a range of proteins associated with the Nrf2/ARE pathway (Nrf2, HO-1, NQO-1, SOD). The CCK-8 assay was used to determine cell survival rates while Co-IP was used to determine the interactions between α2-AR and Nrf2. The TUNEL assay was used to detect the levels of apoptosis in neurons. Results: OGD/R treatment reduced the level of α2-AR protein in neurons and reduced neuronal survival in a time-dependent manner. However, treatment with dexmedetomidine led to an elevation of α2-AR protein expression in OGD/R-treated neurons and the survival rate of OGD/R-treated neurons. These results indicated that dexmedetomidine treatment promoted the viability of OGD/R-treated neurons but inhibited OGD/R-mediated oxidative stress and neuronal apoptosis. From a mechanistic point-of-view, Nrf2 can bind effectively with α2-AR. We believe that dexmedetomidine exerted effect on the Nrf2/ARE pathway in OGD/R-treated neurons. Silencing the expression of Nrf2 reversed the effects of dexmedetomidine on cell viability, oxidative stress, and neuronal apoptosis in OGD/R-treated neurons.Conclusion: Collectively, our data indicate that elucidated that the activation of α2-AR by dexmedetomidine had a protective effect in neurons against OGD/R-triggered oxidative stress and neuronal apoptosis by modulating the Nrf2/ARE pathway, thus providing a novel way forward to develop clinical therapies to reduce oxidative stress induced by neuronal injury.

scholarly journals Quercetin Prevents Diastolic Dysfunction Induced by a High-Cholesterol Diet: Role of Oxidative Stress and Bioenergetics in Hyperglycemic Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Rodrigo L. Castillo ◽  
Emilio A. Herrera ◽  
Alejandro Gonzalez-Candia ◽  
Marjorie Reyes-Farias ◽  
Nicole de la Jara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diastolic Dysfunction ◽  
Nuclear Translocation ◽  
High Cholesterol Diet ◽  
High Cholesterol ◽  
Functional Changes ◽  
Cardioprotective Effects ◽  
Antioxidant Mechanisms ◽  
Antioxidant Enzymatic Activity

Alterations in cardiac energy metabolism play a key role in the pathogenesis of diabetic cardiomyopathy. Hypercholesterolemia associated with bioenergetic impairment and oxidative stress has not been well characterized in the cardiac function under glycemic control deficiency conditions. This work aimed to determine the cardioprotective effects of quercetin (QUE) against the damage induced by a high-cholesterol (HC) diet in hyperglycemic rats, addressing intracellular antioxidant mechanisms and bioenergetics. Quercetin reduced HC-induced alterations in the lipid profile and glycemia in rats. In addition, QUE attenuated cardiac diastolic dysfunction (increased E:A ratio), prevented cardiac cholesterol accumulation, and reduced the increase in HC-induced myocyte density. Moreover, QUE reduced HC-induced oxidative stress by preventing the decrease in GSH/GSSG ratio, Nrf2 nuclear translocation, HO-1 expression, and antioxidant enzymatic activity. Quercetin also counteracted HC-induced bioenergetic impairment, preventing a reduction in ATP levels and alterations in PGC-1α, UCP2, and PPARγ expression. In conclusion, the mechanisms that support the cardioprotective effect of QUE in rats with HC might be mediated by the upregulation of antioxidant mechanisms and improved bioenergetics on the heart. Targeting bioenergetics with QUE can be used as a pharmacological approach to modulate structural and functional changes of the heart under hypercholesterolemic and hyperglycemic conditions.

scholarly journals Implications of Oxidative Stress and Potential Role of Mitochondrial Dysfunction in COVID-19: Therapeutic Effects of Vitamin D

Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 897 ◽  
Author(s):  
Natalia de las Heras ◽  
Virna Margarita Martín Giménez ◽  
León Ferder ◽  
Walter Manucha ◽  
Vicente Lahera
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Cytokine Production ◽  
Mitochondrial Dynamics ◽  
World Population ◽  
Therapeutic Effects ◽  
Worst Case ◽  
The World ◽  
Inflammatory State

Due to its high degree of contagiousness and like almost no other virus, SARS-CoV-2 has put the health of the world population on alert. COVID-19 can provoke an acute inflammatory process and uncontrolled oxidative stress, which predisposes one to respiratory syndrome, and in the worst case, death. Recent evidence suggests the mechanistic role of mitochondria and vitamin D in the development of COVID-19. Indeed, mitochondrial dynamics contribute to the maintenance of cellular homeostasis, and its uncoupling involves pathological situations. SARS-CoV-2 infection is associated with altered mitochondrial dynamics with consequent oxidative stress, pro-inflammatory state, cytokine production, and cell death. Furthermore, vitamin D deficiency seems to be associated with increased COVID-19 risk. In contrast, vitamin D can normalize mitochondrial dynamics, which would improve oxidative stress, pro-inflammatory state, and cytokine production. Furthermore, vitamin D reduces renin–angiotensin–aldosterone system activation and, consequently, decreases ROS generation and improves the prognosis of SARS-CoV-2 infection. Thus, the purpose of this review is to deepen the knowledge about the role of mitochondria and vitamin D directly involved in the regulation of oxidative stress and the inflammatory state in SARS-CoV-2 infection. As future prospects, evidence suggests enhancing the vitamin D levels of the world population, especially of those individuals with additional risk factors that predispose to the lethal consequences of SARS-CoV-2 infection.

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