Role of Oxidative Stress in Diabetic Retinopathy and the Beneficial Effects of Flavonoids

2018 ◽  
Vol 24 (19) ◽  
pp. 2180-2187 ◽  
Author(s):  
Mohammad Shamsul Ola ◽  
Dalia Al-Dosari ◽  
Abdullah S. Alhomida
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Experimental Studies ◽  
Developed Countries ◽  
Retinal Damage ◽  
Beneficial Effects ◽  
Diabetic Retina ◽  
Retinal Pathology ◽  
Dietary Flavonoids

Diabetic Retinopathy (DR) is one of the leading causes of decreased vision and blindness in developed countries. Diabetes-induced metabolic disorder is believed to increase oxidative stress in the retina. This results in deleterious change through dysregulation of cellular physiology that damages both neuronal and vascular cells. In this review, we first highlight the evidence of potential metabolic sources and pathways which increase oxidative stress that contribute to retinal pathology in diabetes. As oxidative stress is a central factor in the pathophysiology of DR, antioxidants therapy would be beneficial towards preventing the retinal damage. A number of experimental studies by our group and others showed that dietary flavonoids cause reduction in increased oxidative stress and other beneficial effects in diabetic retina. We then discuss the beneficial effects of the six major flavonoid families, such as flavanones, flavanols, flavonols, isoflavones, flavones and anthocyanins, which have been studied to improve retinal damage. Flavanoids, being known antioxidants, may ameliorate the retinal degenerative factors including apoptosis, inflammation and neurodegeneration in diabetes. Therefore, intake of potential dietary flavonoids would limit oxidative stress and thereby prevent the retinal damage, and subsequently the development of DR.

The Role of Antioxidants in the Prevention of Cadmium-Induced Endothelial Dysfunction

2020 ◽  
Vol 26 (30) ◽  
pp. 3667-3675 ◽  
Author(s):  
Camila Cruz Pereira Almenara ◽  
Thiago F. Oliveira ◽  
Alessandra S. Padilha
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Antioxidant Properties ◽  
Experimental Studies ◽  
Antioxidant Supplementation ◽  
Pubmed Central ◽  
Major Mechanism ◽  
Beneficial Effects ◽  
Cadmium Intoxication

Background: Cadmium is a worldwide spread toxicant that accumulates in tissues and affects many organs, mainly through oxidative damage. Oxidative stress is often associated with cardiovascular diseases and, when it affects vessels, it induces endothelial dysfunction, which, in turn, could precipitate atherosclerosis and hypertension. Therefore, it is reasonable to suggest antioxidant supplementation as a therapy against cadmiuminduced endothelial dysfunction. Objective: This literature review aims to present the mechanisms involving oxidative stress in which cadmium induces endothelial dysfunction and the benefits of antioxidant supplementation as a therapeutic strategy against its harmful effects. Methods: On PubMed Central, articles that contemplated studies on cadmium intoxication and associated oxidative stress with endothelial dysfunction as well as articles that reported the use of antioxidant supplementation in an attempt to prevent or avoid endothelial dysfunction induced by cadmium exposure were selected. Results: Most of the studies that associated cadmium intoxication with endothelial dysfunction suggested oxidative stress as the major mechanism for this damage. Furthermore, experimental studies also revealed that the administration of substances with antioxidant properties, such as ascorbic acid and curcumin, has beneficial effects on the prevention of such dysfunction, reducing reactive oxygen species within the vessels, preventing a reduction in the amount of glutathione and the increase in blood pressure observed in animals exposed to cadmium. Conclusion: Antioxidant therapy demonstrated to be a potential treatment to reduce cardiovascular injuries provoked by cadmium, but more studies are needed to determine the best antioxidant substance and dose to treat or avoid this complication.

scholarly journals Protective Role of Natural and Semi-Synthetic Tocopherols on TNFα-Induced ROS Production and ICAM-1 and Cl-2 Expression in HT29 Intestinal Epithelial Cells

Antioxidants ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 160
Author(s):  
Vladana Domazetovic ◽  
Irene Falsetti ◽  
Caterina Viglianisi ◽  
Kristian Vasa ◽  
Cinzia Aurilia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Properties ◽  
Intestinal Barrier ◽  
Protective Role ◽  
Intercellular Adhesion Molecule ◽  
Intestinal Epithelial ◽  
Intercellular Adhesion Molecule 1 ◽  
Beneficial Effects ◽  
Bowel Diseases

Vitamin E, a fat-soluble compound, possesses both antioxidant and non-antioxidant properties. In this study we evaluated, in intestinal HT29 cells, the role of natural tocopherols, α-Toc and δ-Toc, and two semi-synthetic derivatives, namely bis-δ-Toc sulfide (δ-Toc)2S and bis-δ-Toc disulfide (δ-Toc)2S2, on TNFα-induced oxidative stress, and intercellular adhesion molecule-1 (ICAM-1) and claudin-2 (Cl-2) expression. The role of tocopherols was compared to that of N-acetylcysteine (NAC), an antioxidant precursor of glutathione synthesis. The results show that all tocopherol containing derivatives used, prevented TNFα-induced oxidative stress and the increase of ICAM-1 and Cl-2 expression, and that (δ-Toc)2S and (δ-Toc)2S2 are more effective than δ-Toc and α-Toc. The beneficial effects demonstrated were due to tocopherol antioxidant properties, but suppression of TNFα-induced Cl-2 expression seems not only to be related with antioxidant ability. Indeed, while ICAM-1 expression is strongly related to the intracellular redox state, Cl-2 expression is TNFα-up-regulated by both redox and non-redox dependent mechanisms. Since ICAM-1 and Cl-2 increase intestinal bowel diseases, and cause excessive recruitment of immune cells and alteration of the intestinal barrier, natural and, above all, semi-synthetic tocopherols may have a potential role as a therapeutic support against intestinal chronic inflammation, in which TNFα represents an important proinflammatory mediator.

Omentin-1 attenuates glucocorticoid-induced cardiac injury by phosphorylating GSK3β

2021 ◽  
Vol 66 (4) ◽  
pp. 273-283
Author(s):  
Zhousheng Jin ◽  
Fangfang Xia ◽  
Jiaojiao Dong ◽  
Tingting Lin ◽  
Yaoyao Cai ◽  
...  
Keyword(s):  
Side Effects ◽  
Cardiac Hypertrophy ◽  
Cardiac Injury ◽  
Experimental Studies ◽  
Chronic Administration ◽  
Cardiovascular Complications ◽  
Rat Serum ◽  
Cardiac Side Effects ◽  
Beneficial Effects

Glucocorticoid excess often causes a variety of cardiovascular complications, including hypertension, atherosclerosis, and cardiac hypertrophy. To abrogate its cardiac side effects, it is necessary to fully disclose the pathophysiological role of glucocorticoid in cardiac remodelling. Previous clinical and experimental studies have found that omentin-1, one of the adipokines, has beneficial effects in cardiovascular diseases, and is closely associated with metabolic disorders. However, there is no evidence to address the potential role of omentin-1 in glucocorticoid excess-induced cardiac injuries. To uncover the links, the present study utilized rat model with glucocorticoid-induced cardiac injuries and clinical patients with abnormal cardiac function. Chronic administration of glucocorticoid excess reduced rat serum omentin-1 concentration, which closely correlated with cardiac functional parameters. Intravenous administration of adeno-associated virus encoding omentin-1 upregulated the circulating omentin-1 level and attenuated glucocorticoid excess-induced cardiac hypertrophy and functional disorders. Overexpression of omentin-1 also improved cardiac mitochondrial function, including the reduction of lipid deposits, induction of mitochondrial biogenesis, and enhanced mitochondrial activities. Mechanistically, omentin-1 phosphorylated and activated the GSK3β pathway in the heart. From a study of 28 patients with Cushing’s syndrome and 23 healthy subjects, the plasma level of glucocorticoid was negatively correlated with omentin-1, and was positively associated with cardiac ejection fraction and fractional shortening. Collectively, the present study provided a novel role of omentin-1 in glucocorticoid excess-induced cardiac injuries and found that the omentin-1/GSK3β pathway was a potential therapeutic target in combating the side effects of glucocorticoid.

scholarly journals Notoginsenoside R1 Ameliorates Diabetic Retinopathy through PINK1-Dependent Activation of Mitophagy

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 213 ◽  
Author(s):  
Ping Zhou ◽  
Weijie Xie ◽  
Xiangbao Meng ◽  
Yadong Zhai ◽  
Xi Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Oral Treatment ◽  
Müller Cells ◽  
Panax Notoginseng ◽  
Protective Effects ◽  
Muller Cells ◽  
Beneficial Effects ◽  
Pre Treatment ◽  
Lc3 Puncta

: Accumulating evidence has indicated that inflammation, oxidative stress, apoptosis, and autophagy in retinal Müller cells are involved in diabetic retinopathy (DR). Notoginsenoside R1 (NGR1), a novel saponin extracted from Panax notoginseng, posesses pharmacological properties, including treating diabetic encephalopathy and improving microcirculatory disorders. Nevertheless, its beneficial effects on DR and the potential mechanism remain to be elucidated. In this study, we found retinal vascular degeneration, reduced retinal thickness, and impaired retinal function in db/db mice were all dramatically attenuated by oral treatment with NGR1 (30 mg/kg) for 12 weeks. NGR1 pretreatment also significantly inhibited apoptosis, markedly suppressed the VEGF expression, markedly increased PEDF expression and markedly inhibited oxidative stress and inflammation in rat retinal Müller cells (rMC-1) subjected to high glucose (HG) and in the retinas of db/db mice. Furthermore, NGR1 pre-treatment upregulated the level of PINK1 and Parkin, increased the LC3-II/LC3-I ratio, and downregulated the level of p62/SQSTM1 in rMC-1 cells induced by HG and in the retinas of db/db mice. Moreover, NGR1 administration enhanced the co-localization of GFP-LC3 puncta and MitoTracker in rMC-1 cells. Importantly, knockdown of PINK1 abolished the protective effects of NGR1. In conclusion, these phenomena suggested that NGR1 prevented DR via PINK1-dependent enhancement of mitophagy.

scholarly journals The Role of Oxidative Stress in Cardiac Disease: From Physiological Response to Injury Factor

2020 ◽  
Vol 2020 ◽  
pp. 1-29 ◽  
Author(s):  
Rossella D’Oria ◽  
Rossella Schipani ◽  
Anna Leonardini ◽  
Annalisa Natalicchio ◽  
Sebastio Perrini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Injury ◽  
Antioxidant Defense ◽  
Experimental Studies ◽  
Chemical Species ◽  
Oxygen Species ◽  
Molecular Abnormalities ◽  
Defense Systems ◽  
Antioxidant Defense Systems

Reactive oxygen species (ROS) are highly reactive chemical species containing oxygen, controlled by both enzymatic and nonenzymatic antioxidant defense systems. In the heart, ROS play an important role in cell homeostasis, by modulating cell proliferation, differentiation, and excitation-contraction coupling. Oxidative stress occurs when ROS production exceeds the buffering capacity of the antioxidant defense systems, leading to cellular and molecular abnormalities, ultimately resulting in cardiac dysfunction. In this review, we will discuss the physiological sources of ROS in the heart, the mechanisms of oxidative stress-related myocardial injury, and the implications of experimental studies and clinical trials with antioxidant therapies in cardiovascular diseases.

The Role of Nrf2 in D-Galactose-Induced Cardiac Aging in Mice: Involvement of Oxidative Stress

Gerontology ◽  
2020 ◽  
pp. 1-10
Author(s):  
Xilan Yang ◽  
Jian Jia ◽  
Ling Ding ◽  
Zhen Yu ◽  
Chen Qu
Keyword(s):  
Oxidative Stress ◽  
Developed Countries ◽  
Antioxidative Effect ◽  
Cardiac Aging ◽  
Detailed Mechanism ◽  
Candidate Drug ◽  
Nrf2 Activator ◽  
And Oxidative Stress ◽  
Aging Cell

<b><i>Introduction:</i></b> Cardiac aging is the major risk factor for advanced heart disease, which is the leading cause of death in developed countries, accounting for &#x3e;30% of deaths worldwide. <b><i>Objective:</i></b> To discover the detailed mechanism of cardiac aging and develop an effective therapeutic candidate drug to treat or delay cardiac aging. <b><i>Methods:</i></b> We used D-galactose to induce cardiac aging in Nrf2<sup>+/+</sup> and Nrf2<sup>–/–</sup> mice, and then treated these mice with vehicle or the Nrf2 activator, CDDO-imidazolide (CDDO-Im). <b><i>Results and Conclusions:</i></b> D-galactose injection significantly induced cardiac aging, cell apoptosis, and oxidative stress in Nrf2<sup>+/+</sup> mice, all of which were further exacerbated in Nrf2<sup>–/–</sup> mice. CDDO-Im treatment can effectively weaken oxidative stress and enhance the activities of antioxidant enzymes, but CDDO-Im lost its antioxidative effect in the Nrf2<sup>–/–</sup> mice. Nrf2 activator CDDO-Im could therefore effectively protect against D-galactose-induced cardiac aging by inhibiting oxidative stress, suggesting that CDDO-Im might be a potential and promising therapeutic candidate drug to treat cardiac aging.

scholarly journals Neural Underpinnings of Obesity: The Role of Oxidative Stress and Inflammation in the Brain

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 1018
Author(s):  
Caitlyn A. Mullins ◽  
Ritchel B. Gannaban ◽  
Md Shahjalal Khan ◽  
Harsh Shah ◽  
Md Abu B. Siddik ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Homeostasis ◽  
Dorsal Striatum ◽  
Brain Regions ◽  
Therapeutic Interventions ◽  
Low Grade ◽  
Obesity Prevalence ◽  
Beneficial Effects ◽  
The Brain

Obesity prevalence is increasing at an unprecedented rate throughout the world, and is a strong risk factor for metabolic, cardiovascular, and neurological/neurodegenerative disorders. While low-grade systemic inflammation triggered primarily by adipose tissue dysfunction is closely linked to obesity, inflammation is also observed in the brain or the central nervous system (CNS). Considering that the hypothalamus, a classical homeostatic center, and other higher cortical areas (e.g. prefrontal cortex, dorsal striatum, hippocampus, etc.) also actively participate in regulating energy homeostasis by engaging in inhibitory control, reward calculation, and memory retrieval, understanding the role of CNS oxidative stress and inflammation in obesity and their underlying mechanisms would greatly help develop novel therapeutic interventions to correct obesity and related comorbidities. Here we review accumulating evidence for the association between ER stress and mitochondrial dysfunction, the main culprits responsible for oxidative stress and inflammation in various brain regions, and energy imbalance that leads to the development of obesity. Potential beneficial effects of natural antioxidant and anti-inflammatory compounds on CNS health and obesity are also discussed.

scholarly journals The Role of Date Palm (Phoenix dactylifera L) Pollen in Fertility

2016 ◽  
Vol 21 (4) ◽  
pp. 320-324 ◽  
Author(s):  
Mohammad Tahvilzadeh ◽  
Mannan Hajimahmoodi ◽  
Roja Rahimi
Keyword(s):  
Date Palm ◽  
Experimental Studies ◽  
Phoenix Dactylifera ◽  
Beneficial Effects ◽  
Reproductive Effects ◽  
Phoenix Dactylifera L ◽  
Comprehensive Information ◽  
Ancient Times ◽  
Fertility Disorders

Date palm pollen (DPP) is the male reproductive dust of palm flowers used as dietary supplement especially as aphrodisiac and fertility enhancer in both women and men from ancient times. Although there are few clinical trials evaluating the beneficial effects of DPP in humans, various experimental studies have been conducted on the reproductive effects of DPP. Among the compounds isolated from DPP are amino acids, fatty acids, flavonoids, saponins, and estroles. The present review summarizes comprehensive information concerning the phytochemistry and pharmacological activities of DPP and its application in fertility disorders.

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