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Antioxidants
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Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases
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Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (15 March 2022) | Viewed by 60275

Special Issue Editors

Dr. Yi-Sook Jung

E-Mail Website
Guest Editor
College of Pharmacy, Ajou University, Suwon 16499, Republic of Korea
Interests: natural product; ROS; vascular pathophysiology; platelet; dementia
Special Issues, Collections and Topics in MDPI journals
Dr. Sang Hee Shim

E-Mail Website
Guest Editor
School of Pharmacy, Duksung Women’s University, Seoul 01369, Korea
Interests: natural products; secondary metabolite; ROS; atherosclerosis; vascular disease
Dr. Dong Hyun Kim

E-Mail Website
Guest Editor
Department of Pharmacology and Department of Advanced Translational Medicine, School of Medicine, Konkuk University, Seoul 05029, Korea
Interests: natural antioxidants; cerebrovascular disease

Special Issue Information

Dear Colleagues,

Natural antioxidants are widely distributed in food and medicinal plants, and differ in their composition, physical and chemical properties. Owing to their diverse components, they exhibit a wide spectrum of biological effects and mechanisms of action, and have been a productive source of lead compounds for the development of novel therapeutics.

Oxidative stress causes damage to proteins, lipids and DNA, and occurs when ROS accumulate in cells due to an imbalance between ROS production and the antioxidant system. Numerous studies have demonstrated that ROS play a crucial role in the pathophysiology of a variety of diseases, including cardiovascular and cerebrovascular diseases, which are regarded as one of the major causes of mortality worldwide.

This Special Issue focuses on new findings related to natural antioxidants and their relevance to cardiovascular and cerebrovascular diseases. This issue also welcomes contributions on the role of ROS at the cellular level, providing more knowledge about oxidative damage mechanisms in cells, organelles and signaling molecules. Authors are invited to submit both original research papers and review articles.

Dr. Yi-Sook Jung
Dr. Sang Hee Shim
Dr. Dong Hyun Kim
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Natural antioxidant
  • Oxidative stress
  • Reactive oxygen species
  • Cardiovascular disease
  • Cerebrovascular disease

Published Papers (17 papers)

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Editorial

Jump to: Research, Review

3 pages, 185 KiB  
Editorial
Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases
by Yi-Sook Jung
Antioxidants 2022, 11(6), 1159; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11061159 - 13 Jun 2022
Cited by 2 | Viewed by 1261
Abstract
Cardiovascular (CVD) and cerebrovascular diseases, with 17 [...] Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)

Research

Jump to: Editorial, Review

24 pages, 8904 KiB  
Article
Effects of Gold Nanoparticles Functionalized with Bioactive Compounds from Cornus mas Fruit on Aorta Ultrastructural and Biochemical Changes in Rats on a Hyperlipid Diet—A Preliminary Study
by Remus Moldovan, Daniela-Rodica Mitrea, Adrian Florea, Irina-Camelia Chiş, Şoimiţa Suciu, Luminiţa David, Bianca Elena Moldovan, Laura Elena Mureşan, Manuela Lenghel, Rodica Ana Ungur, Răzvan Vlad Opriş, Nicoleta Decea and Simona Valeria Clichici
Antioxidants 2022, 11(7), 1343; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11071343 - 08 Jul 2022
Cited by 7 | Viewed by 1983
Abstract
Cornus mas L. extract (CM) presents hypolipidemic, antioxidant and anti-inflammatory activity. Gold nanoparticles (AuNPs) are considered potent delivery systems and may be used to release pharmaceutical compounds at the level of injury. In our study, we used gold nanoparticles functionalized with bioactive compounds [...] Read more.
Cornus mas L. extract (CM) presents hypolipidemic, antioxidant and anti-inflammatory activity. Gold nanoparticles (AuNPs) are considered potent delivery systems and may be used to release pharmaceutical compounds at the level of injury. In our study, we used gold nanoparticles functionalized with bioactive compounds from Cornus mas L. (AuNPsCM) in an experimental model of a high-fat diet (HFD), and we assessed their effects on aorta wall but also in the serum, as compared to Cornus mas (CM) administration. Sprague Dawley female rats were fed for 9 months with an HFD. During the last month of the experiment, we randomly allocated the animals into three groups that received, by oral gavage: saline solution, CM solution (0.158 mg/mL polyphenols) or AuNPsCM solution (260 μg Au/kg/day), while a Control group received a standard diet and saline solution. At the end of the experiment, we performed an ultrasonography of the aorta and left ventricle and a histology and transmission electron microscopy of the aorta walls; we investigated the oxidative stress and inflammation in aorta homogenates and in serum and, in addition, the lipid profile. AuNPsCM presented better effects in comparison with the natural extract (CM) on lipid peroxidation (p < 0.01) and TNF-alpha (p < 0.001) in aorta homogenates. In serum, both CM and AuNPsCM decreased the triglycerides (p < 0.001) and C-reactive protein (CM, p < 0.01; AuNPsCM, p < 0.001) and increased the antioxidant protection (p < 0.001), in comparison with the HFD group. In intima, AuNPsCM produced ultrastructural lesions, with the disorganization of intima and subendothelial connective layer, whereas CM administration preserved the intima normal aspect, but with a thinned subendothelial connective layer. AuNPsCM oral administration presented certain antioxidant, anti-inflammatory and hypolipidemic effects in an experimental model of HFD, but with a negative impact on the ultrastructure of aorta walls, highlighted by the intima disorganization. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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14 pages, 1603 KiB  
Article
Epigallocatechin Gallate Modulates Essential Elements, Zn/Cu Ratio, Hazardous Metal, Lipid Peroxidation, and Antioxidant Activity in the Brain Cortex during Cerebral Ischemia
by Ming-Cheng Lin, Chien-Chi Liu, Yu-Chen Lin and Ching-Wen Hsu
Antioxidants 2022, 11(2), 396; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020396 - 16 Feb 2022
Cited by 7 | Viewed by 2190
Abstract
Cerebral ischemia induces oxidative brain injury via increased oxidative stress. Epigallocatechin gallate (EGCG) exerts anti-oxidant, anti-inflammatory, and metal chelation effects through its active polyphenol constituent. This study investigates whether EGCG protection against cerebral ischemia-induced brain cortex injury occurs through modulating lipid peroxidation, antioxidant [...] Read more.
Cerebral ischemia induces oxidative brain injury via increased oxidative stress. Epigallocatechin gallate (EGCG) exerts anti-oxidant, anti-inflammatory, and metal chelation effects through its active polyphenol constituent. This study investigates whether EGCG protection against cerebral ischemia-induced brain cortex injury occurs through modulating lipid peroxidation, antioxidant activity, the essential elements of selenium (Se), zinc (Zn), magnesium (Mg), copper (Cu), iron (Fe), and copper (Cu), Zn/Cu ratio, and the hazardous metal lead (Pb). Experimentally, assessment of the ligation group was performed by occlusion of the right common carotid artery and the right middle cerebral artery for 1 h. The prevention group was intraperitoneally injected with EGCG (50 mg/kg) once daily for 10 days before cerebral ischemia. The brain cortex tissues were homogenized and the supernatants were harvested for biochemical analysis. Results indicated that cerebral ischemia markedly decreased SOD, CAT, Mg, Zn, Se, and Zn/Cu ratio and increased malondialdehyde (MDA), Fe, Cu, and Pb in the ischemic brain cortex. Notably, pretreating rats with EGCG before ischemic injury significantly reversed these biochemical results. Our findings suggest that the neuroprotection of EGCG in the ischemic brain cortex during cerebral ischemia involves attenuating oxidative injury. Notably, this neuroprotective mechanism is associated with regulating lipid peroxidation, antioxidant activity, essential elements, Zn/Cu ratio, and hazardous metal Pb. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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13 pages, 2936 KiB  
Article
Aβ1–40-Induced Platelet Adhesion Is Ameliorated by Rosmarinic Acid through Inhibition of NADPH Oxidase/PKC-δ/Integrin αIIbβ3 Signaling
by Bo Kyung Lee, Hye Jin Jee and Yi-Sook Jung
Antioxidants 2021, 10(11), 1671; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10111671 - 23 Oct 2021
Cited by 7 | Viewed by 2356
Abstract
In platelets, oxidative stress reportedly increases platelet adhesion to vessels, thus promoting the vascular pathology of various neurodegenerative diseases, including Alzheimer’s disease (AD). Recently, it has been shown that β-amyloid (Aβ) can increase oxidative stress in platelets; however, the underlying mechanism remains elusive. [...] Read more.
In platelets, oxidative stress reportedly increases platelet adhesion to vessels, thus promoting the vascular pathology of various neurodegenerative diseases, including Alzheimer’s disease (AD). Recently, it has been shown that β-amyloid (Aβ) can increase oxidative stress in platelets; however, the underlying mechanism remains elusive. In the present study, we aimed to elucidate the signaling pathway of platelet adhesion induced by Aβ1–40, the major form of circulating Aβ, through Western blotting, immunofluorescence confocal microscopy, and fluorescence-activated cell sorting analysis. Additionally, we examined whether rosmarinic acid (RA), a natural polyphenol antioxidant, can modulate these processes. Our results show that Aβ1–40-induced platelet adhesion is mediated through NADPH oxidase/ROS/PKC-δ/integrin αIIbβ3 signaling, and these signaling pathways are significantly inhibited by RA. Collectively, these results suggest that RA may have beneficial effects on platelet-associated vascular pathology in AD. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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Graphical abstract

22 pages, 8307 KiB  
Article
Histochrome Attenuates Myocardial Ischemia-Reperfusion Injury by Inhibiting Ferroptosis-Induced Cardiomyocyte Death
by Ji-Won Hwang, Jae-Hyun Park, Bong-Woo Park, Hyeok Kim, Jin-Ju Kim, Woo-Sup Sim, Natalia P. Mishchenko, Sergey A. Fedoreyev, Elena A. Vasileva, Kiwon Ban, Hun-Jun Park and Sang-Hong Baek
Antioxidants 2021, 10(10), 1624; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10101624 - 15 Oct 2021
Cited by 38 | Viewed by 3933
Abstract
Reactive oxygen species (ROS) and intracellular iron levels are critical modulators of lipid peroxidation that trigger iron-dependent non-apoptotic ferroptosis in myocardial ischemia-reperfusion (I/R) injury. Histochrome (HC), with a potent antioxidant moiety and iron-chelating capacity, is now available in clinical practice. However, limited data [...] Read more.
Reactive oxygen species (ROS) and intracellular iron levels are critical modulators of lipid peroxidation that trigger iron-dependent non-apoptotic ferroptosis in myocardial ischemia-reperfusion (I/R) injury. Histochrome (HC), with a potent antioxidant moiety and iron-chelating capacity, is now available in clinical practice. However, limited data are available about the protective effects of HC on ferroptotic cell death in myocardial I/R injury. In this study, we investigated whether the intravenous administration of HC (1 mg/kg) prior to reperfusion could decrease myocardial damage by reducing ferroptosis. Rats undergoing 60 min of ischemia and reperfusion were randomly divided into three groups as follows: (1) Sham, (2) I/R control, and (3) I/R + HC. Serial echocardiography up to four weeks after I/R injury showed that intravenous injection of HC significantly improved cardiac function compared to the I/R controls. In addition, the hearts of rats who received intravenous injection of HC exhibited significantly lower cardiac fibrosis and higher capillary density. HC treatment decreased intracellular and mitochondrial ROS levels by upregulating the expression of nuclear factor erythroid 2-related factor (Nrf2) and its downstream genes. HC also inhibited erastin- and RSL3-induced ferroptosis in rat neonatal cardiomyocytes by maintaining the intracellular glutathione level and through upregulated activity of glutathione peroxidase 4. These findings suggest that early intervention with HC before reperfusion rescued myocardium from I/R injury by preventing ferroptotic cell death. Therefore, HC is a promising therapeutic option to provide secondary cardioprotection in patients who undergo coronary reperfusion therapy. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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13 pages, 2334 KiB  
Article
Auraptene Enhances Junction Assembly in Cerebrovascular Endothelial Cells by Promoting Resilience to Mitochondrial Stress through Activation of Antioxidant Enzymes and mtUPR
by Min Joung Lee, Yunseon Jang, Jiebo Zhu, Eunji Namgung, Dahyun Go, Changjun Seo, Xianshu Ju, Jianchen Cui, Yu Lim Lee, Hyoeun Kang, Hyeongseok Kim, Woosuk Chung and Jun Young Heo
Antioxidants 2021, 10(3), 475; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030475 - 17 Mar 2021
Cited by 11 | Viewed by 2732
Abstract
Junctional proteins in cerebrovascular endothelial cells are essential for maintaining the barrier function of the blood-brain barrier (BBB), thus protecting the brain from the infiltration of pathogens. The present study showed that the potential therapeutic natural compound auraptene (AUR) enhances junction assembly in [...] Read more.
Junctional proteins in cerebrovascular endothelial cells are essential for maintaining the barrier function of the blood-brain barrier (BBB), thus protecting the brain from the infiltration of pathogens. The present study showed that the potential therapeutic natural compound auraptene (AUR) enhances junction assembly in cerebrovascular endothelial cells by inducing antioxidant enzymes and the mitochondrial unfolded protein response (mtUPR). Treatment of mouse cerebrovascular endothelial cells with AUR enhanced the expression of junctional proteins, such as occludin, zonula occludens-1 (ZO-1) and vascular endothelial cadherin (VE-cadherin), by increasing the levels of mRNA encoding antioxidant enzymes. AUR treatment also resulted in the depolarization of mitochondrial membrane potential and activation of mtUPR. The ability of AUR to protect against ischemic conditions was further assessed using cells deprived of oxygen and glucose. Pretreatment of these cells with AUR protected against damage to junctional proteins, including occludin, claudin-5, ZO-1 and VE-cadherin, accompanied by a stress resilience response regulated by levels of ATF5, LONP1 and HSP60 mRNAs. Collectively, these results indicate that AUR promotes resilience against oxidative stress and improves junction assembly, suggesting that AUR may help maintain intact barriers in cerebrovascular endothelial cells. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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16 pages, 2358 KiB  
Article
Taurine Protects against Postischemic Brain Injury via the Antioxidant Activity of Taurine Chloramine
by Song-I Seol, Hyun Jae Kim, Eun Bi Choi, In Soon Kang, Hye-Kyung Lee, Ja-Kyeong Lee and Chaekyun Kim
Antioxidants 2021, 10(3), 372; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030372 - 02 Mar 2021
Cited by 16 | Viewed by 3185
Abstract
Taurine is ubiquitously distributed in mammalian tissues and is highly concentrated in the heart, brain, and leukocytes. Taurine exerts neuroprotective effects in various central nervous system diseases and can suppress infarct formation in stroke. Taurine reacts with myeloperoxidase (MPO)-derived hypochlorous acid (HOCl) to [...] Read more.
Taurine is ubiquitously distributed in mammalian tissues and is highly concentrated in the heart, brain, and leukocytes. Taurine exerts neuroprotective effects in various central nervous system diseases and can suppress infarct formation in stroke. Taurine reacts with myeloperoxidase (MPO)-derived hypochlorous acid (HOCl) to produce taurine chloramine (Tau-Cl). We investigated the neuroprotective effects of taurine using a rat middle cerebral artery occlusion (MCAO) model and BV2 microglial cells. Although intranasal administration of taurine (0.5 mg/kg) had no protective effects, the same dose of Tau-Cl significantly reduced infarct volume and ameliorated neurological deficits and promoted motor function, indicating a robust neuroprotective effect of Tau-Cl. There was neutrophil infiltration in the post-MCAO brains, and the MPO produced by infiltrating neutrophils might be involved in the taurine to Tau-Cl conversion. Tau-Cl significantly increased the levels of antioxidant enzymes glutamate–cysteine ligase, heme oxygenase-1, NADPH:quinone oxidoreductase 1, and peroxiredoxin-1 in BV2 cells, whereas taurine slightly increased some of them. Antioxidant enzyme levels were increased in the post-MCAO brains, and Tau-Cl further increased the level of MCAO-induced antioxidant enzymes. These results suggest that the neutrophils infiltrate the area of ischemic injury area, where taurine is converted to Tau-Cl, thus protecting from brain injury by scavenging toxic HOCl and increasing antioxidant enzyme expression. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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Graphical abstract

15 pages, 1951 KiB  
Article
Prevention of Fine Dust-Induced Vascular Senescence by Humulus lupulus Extract and Its Major Bioactive Compounds
by Saugat Shiwakoti, Deepak Adhikari, Jeong Pyo Lee, Ki-Woon Kang, Ik-Soo Lee, Hyun Jung Kim and Min-Ho Oak
Antioxidants 2020, 9(12), 1243; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9121243 - 07 Dec 2020
Cited by 12 | Viewed by 2448
Abstract
Both short- and long-term exposure to fine dust (FD) from air pollution has been linked to various cardiovascular diseases (CVDs). Endothelial cell (EC) senescence is an important risk factor for CVDs, and recent evidence suggests that FD-induced premature EC senescence increases oxidative stress [...] Read more.
Both short- and long-term exposure to fine dust (FD) from air pollution has been linked to various cardiovascular diseases (CVDs). Endothelial cell (EC) senescence is an important risk factor for CVDs, and recent evidence suggests that FD-induced premature EC senescence increases oxidative stress levels. Hop plant (Humulus lupulus) is a very rich source of polyphenols known to have nutritional and therapeutic properties, including antioxidant behavior. The aims of this study were to evaluate whether Humulus lupulus extract prevents FD-induced vascular senescence and dysfunction and, if so, to characterize the underlying mechanisms and active components. Porcine coronary arteries and endothelial cells were treated with FD in the presence or absence of hop extract (HOP), and the senescence-associated-beta galactosidase (SA-β-gal) activity, cell-cycle progression, expression of senescence markers, oxidative stress level, and vascular function were evaluated. Results indicated that HOP inhibited FD-induced SA-β-gal activity, cell-cycle arrest, and oxidative stress, suggesting that HOP prevents premature induction of senescence by FD. HOP also ameliorated FD-induced vascular dysfunction. Additionally, xanthohumol (XN) and isoxanthohumol (IX) were found to produce the protective effects of HOP. Treatment with HOP and its primary active components XN and IX downregulated the expression of p22phox, p53, and angiotensin type 1 receptor, which all are known FD-induced redox-sensitive EC senescence inducers. Taken together, HOP and its active components protect against FD-induced endothelial senescence most likely via antioxidant activity and may be a potential therapeutic agent for preventing and/or treating air-pollution-associated CVDs. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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17 pages, 3019 KiB  
Article
Sinapic Acid Inhibits Cardiac Hypertrophy via Activation of Mitochondrial Sirt3/SOD2 Signaling in Neonatal Rat Cardiomyocytes
by Ui Jeong Yun and Dong Kwon Yang
Antioxidants 2020, 9(11), 1163; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9111163 - 21 Nov 2020
Cited by 19 | Viewed by 2921
Abstract
Sinapic acid (SA) is a naturally occurring phenolic compound with antioxidant properties. It also has a wide range of pharmacological properties, such as anti-inflammatory, anticancer, and hepatoprotective properties. The present study aimed to evaluate the potential pharmacological effects of SA against hypertrophic responses [...] Read more.
Sinapic acid (SA) is a naturally occurring phenolic compound with antioxidant properties. It also has a wide range of pharmacological properties, such as anti-inflammatory, anticancer, and hepatoprotective properties. The present study aimed to evaluate the potential pharmacological effects of SA against hypertrophic responses in neonatal rat cardiomyocytes. In order to evaluate the preventive effect of SA on cardiac hypertrophy, phenylephrine (PE)-induced hypertrophic cardiomyocytes were treated with subcytotoxic concentrations of SA. SA effectively suppressed hypertrophic responses, such as cell size enlargement, sarcomeric rearrangement, and fetal gene re-expression. In addition, SA significantly inhibited the expression of mitogen-activated protein kinase (MAPK) proteins as pro-hypertrophic factors and protected the mitochondrial functions from hypertrophic stimuli. Notably, SA activated Sirt3, a mitochondrial deacetylase, and SOD2, a mitochondrial antioxidant, in hypertrophic cardiomyocytes. SA also inhibited oxidative stress in hypertrophic cardiomyocytes. However, the protective effect of SA was significantly reduced in Sirt3-silenced hypertrophic cardiomyocytes, indicating that SA exerts its beneficial effect through Sirt3/SOD signaling. In summary, this is the first study to reveal the potential pharmacological action and inhibitory mechanism of SA as an antioxidant against cardiac hypertrophy, suggesting that SA could be utilized for the treatment of cardiac hypertrophy. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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15 pages, 4441 KiB  
Article
Neuroprotective Effect of Tricyclic Pyridine Alkaloids from Fusarium lateritium SSF2, against Glutamate-Induced Oxidative Stress and Apoptosis in the HT22 Hippocampal Neuronal Cell Line
by Dahae Lee, Hyun Gyu Choi, Ji Hye Hwang, Sang Hee Shim and Ki Sung Kang
Antioxidants 2020, 9(11), 1115; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9111115 - 11 Nov 2020
Cited by 14 | Viewed by 3193
Abstract
Excessive glutamate damages neuronal cells via the accumulation of intracellular reactive oxygen species (ROS), calcium ion (Ca2+) influx, depolarization of mitochondrial membrane potential, and apoptosis, which may result in the development of chronic neurodegenerative diseases. In this study, we evaluated the [...] Read more.
Excessive glutamate damages neuronal cells via the accumulation of intracellular reactive oxygen species (ROS), calcium ion (Ca2+) influx, depolarization of mitochondrial membrane potential, and apoptosis, which may result in the development of chronic neurodegenerative diseases. In this study, we evaluated the effects of 4,6′-anhydrooxysporidinone isolated from endophytic fungus Fusarium lateritium SSF2 on glutamate-induced cytotoxicity, accumulation of intracellular ROS, increases in superoxide anion production, Ca2+, depolarization of mitochondrial membrane potential, and apoptotic cell death in hippocampal HT22 cells. 2′,7′-Dichlorofluorescin diacetate (H2DCFDA) staining was used to determine the intracellular reactive oxygen species concentration and dihydroethidine (DHE) staining was used to determine the superoxide radical. Expression of the nuclear factor-erythroid-2–related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) was analyzed by Western blot. Fluo-4 staining was used to determine the intracellular Ca2+ levels. In order to explore mitochondrial membrane potential, tetramethylrhodamine methyl ester (TMRM) staining was used. Apoptotic cell death was evaluated using Annexin-V/propidium iodide (PI) staining and TUNEL staining. Expression of the cytochrome c release and cleaved caspase-9, -3 was analyzed by Western blot. Here, we were able to isolate 4,6′-anhydrooxysporidinone from endophytic fungus, Fusarium lateritium SSF2, which was shown to protect HT22 cells from glutamate-induced cytotoxicity, accumulation of intracellular ROS, increases in superoxide anion production, Ca2+, and depolarization of mitochondrial membrane potential. In addition, 4,6′-anhydrooxysporidinone enhanced the expressions of Nrf2 and HO-1. It also inhibited the apoptotic cell death through the inhibition of cytochrome c release and cleaved caspase-9, -3 in glutamate-treated HT22 cells. Therefore, our results provide ample evidence of the neuroprotective properties of 4,6′-anhydrooxysporidinone. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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15 pages, 12922 KiB  
Article
Yuzu and Hesperidin Ameliorate Blood-Brain Barrier Disruption during Hypoxia via Antioxidant Activity
by Bo Kyung Lee, Soo-Wang Hyun and Yi-Sook Jung
Antioxidants 2020, 9(9), 843; https://doi.org/10.3390/antiox9090843 - 09 Sep 2020
Cited by 22 | Viewed by 3924
Abstract
Yuzu and its main component, hesperidin (HSP), have several health benefits owing to their anti-inflammatory and antioxidant properties. We examined the effects of yuzu and HSP on blood–brain barrier (BBB) dysfunction during ischemia/hypoxia in an in vivo animal model and an in vitro [...] Read more.
Yuzu and its main component, hesperidin (HSP), have several health benefits owing to their anti-inflammatory and antioxidant properties. We examined the effects of yuzu and HSP on blood–brain barrier (BBB) dysfunction during ischemia/hypoxia in an in vivo animal model and an in vitro BBB endothelial cell model, and also investigated the underlying mechanisms. In an in vitro BBB endothelial cell model, BBB permeability was determined by measurement of Evans blue extravasation in vivo and in vitro. The expression of tight junction proteins, such as claudin-5 and zonula occludens-1 (ZO-1), was detected by immunochemistry and western blotting, and the reactive oxygen species (ROS) level was measured by 2′7′-dichlorofluorescein diacetate intensity. Yuzu and HSP significantly ameliorated the increase in BBB permeability and the disruption of claudin-5 and ZO-1 in both in vivo and in vitro models. In bEnd.3 cells, yuzu and HSP were shown to inhibit the disruption of claudin-5 and ZO-1 during hypoxia, and the protective effects of yuzu and HSP on claudin-5 degradation seemed to be mediated by Forkhead box O 3a (FoxO3a) and matrix metalloproteinase (MMP)-3/9. In addition, well-known antioxidants, trolox and N-acetyl cysteine, significantly attenuated the BBB permeability increase, disruption of claudin-5 and ZO-1, and FoxO3a activation during hypoxia, suggesting that ROS are important mediators of BBB dysfunction during hypoxia. Collectively, these results indicate that yuzu and HSP protect the BBB against dysfunction via maintaining integrity of claudin-5 and ZO-1, and these effects of yuzu and HSP appear to be a facet of their antioxidant properties. Our findings may contribute to therapeutic strategies for BBB-associated neurodegenerative diseases. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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Review

Jump to: Editorial, Research

25 pages, 3436 KiB  
Review
Effects of Natural Polyphenols on Oxidative Stress-Mediated Blood-Brain Barrier Dysfunction
by Yeonjae Kim, A Yeon Cho, Hong Cheol Kim, Dajung Ryu, Sangmee Ahn Jo and Yi-Sook Jung
Antioxidants 2022, 11(2), 197; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020197 - 20 Jan 2022
Cited by 25 | Viewed by 3884
Abstract
The blood-brain barrier (BBB), which consists mainly of brain microvascular endothelial cells and astrocytes connected by tight junctions (TJs) and adhesion molecules (AMs), maintains the homeostatic balance between brain parenchyma and extracellular fluid. Accumulating evidence shows that BBB dysfunction is a common feature [...] Read more.
The blood-brain barrier (BBB), which consists mainly of brain microvascular endothelial cells and astrocytes connected by tight junctions (TJs) and adhesion molecules (AMs), maintains the homeostatic balance between brain parenchyma and extracellular fluid. Accumulating evidence shows that BBB dysfunction is a common feature of neurodegenerative diseases, including stroke, traumatic brain injury, and Alzheimer’s disease. Among the various pathological pathways of BBB dysfunction, reactive oxygen species (ROS) are known to play a key role in inducing BBB disruption mediated via TJ modification, AM induction, cytoskeletal reorganization, and matrix metalloproteinase activation. Thus, antioxidants have been suggested to exert beneficial effects on BBB dysfunction-associated brain diseases. In this review, we summarized the sources of ROS production in multiple cells that constitute or surround the BBB, such as BBB endothelial cells, astrocytes, microglia, and neutrophils. We also reviewed various pathological mechanisms by which BBB disruption is caused by ROS in these cells. Finally, we summarized the effects of various natural polyphenols on BBB dysfunction to suggest a therapeutic strategy for BBB disruption-related brain diseases. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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22 pages, 1027 KiB  
Review
Modulations of Cardiac Functions and Pathogenesis by Reactive Oxygen Species and Natural Antioxidants
by Sun-Hee Woo, Joon-Chul Kim, Nipa Eslenur, Tran Nguyet Trinh and Long Nguyen Hoàng Do
Antioxidants 2021, 10(5), 760; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10050760 - 11 May 2021
Cited by 12 | Viewed by 3687
Abstract
Homeostasis in the level of reactive oxygen species (ROS) in cardiac myocytes plays a critical role in regulating their physiological functions. Disturbance of balance between generation and removal of ROS is a major cause of cardiac myocyte remodeling, dysfunction, and failure. Cardiac myocytes [...] Read more.
Homeostasis in the level of reactive oxygen species (ROS) in cardiac myocytes plays a critical role in regulating their physiological functions. Disturbance of balance between generation and removal of ROS is a major cause of cardiac myocyte remodeling, dysfunction, and failure. Cardiac myocytes possess several ROS-producing pathways, such as mitochondrial electron transport chain, NADPH oxidases, and nitric oxide synthases, and have endogenous antioxidation mechanisms. Cardiac Ca2+-signaling toolkit proteins, as well as mitochondrial functions, are largely modulated by ROS under physiological and pathological conditions, thereby producing alterations in contraction, membrane conductivity, cell metabolism and cell growth and death. Mechanical stresses under hypertension, post-myocardial infarction, heart failure, and valve diseases are the main causes for stress-induced cardiac remodeling and functional failure, which are associated with ROS-induced pathogenesis. Experimental evidence demonstrates that many cardioprotective natural antioxidants, enriched in foods or herbs, exert beneficial effects on cardiac functions (Ca2+ signal, contractility and rhythm), myocytes remodeling, inflammation and death in pathological hearts. The review may provide knowledge and insight into the modulation of cardiac pathogenesis by ROS and natural antioxidants. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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22 pages, 1861 KiB  
Review
Molecular Mechanisms Associated with ROS-Dependent Angiogenesis in Lower Extremity Artery Disease
by Greg Hutchings, Łukasz Kruszyna, Mariusz J. Nawrocki, Ewa Strauss, Rut Bryl, Julia Spaczyńska, Bartłomiej Perek, Marek Jemielity, Paul Mozdziak, Bartosz Kempisty, Michał Nowicki and Zbigniew Krasiński
Antioxidants 2021, 10(5), 735; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10050735 - 07 May 2021
Cited by 11 | Viewed by 4596
Abstract
Currently, atherosclerosis, which affects the vascular bed of all vital organs and tissues, is considered as a leading cause of death. Most commonly, atherosclerosis involves coronary and peripheral arteries, which results in acute (e.g., myocardial infarction, lower extremities ischemia) or chronic (persistent ischemia [...] Read more.
Currently, atherosclerosis, which affects the vascular bed of all vital organs and tissues, is considered as a leading cause of death. Most commonly, atherosclerosis involves coronary and peripheral arteries, which results in acute (e.g., myocardial infarction, lower extremities ischemia) or chronic (persistent ischemia leading to severe heart failure) consequences. All of them have a marked unfavorable impact on the quality of life and are associated with increased mortality and morbidity in human populations. Lower extremity artery disease (LEAD, also defined as peripheral artery disease, PAD) refers to atherosclerotic occlusive disease of the lower extremities, where partial or complete obstruction of peripheral arteries is observed. Decreased perfusion can result in ischemic pain, non-healing wounds, and ischemic ulcers, and significantly reduce the quality of life. However, the progressive atherosclerotic changes cause stimulation of tissue response processes, like vessel wall remodeling and neovascularization. These mechanisms of adapting the vascular network to pathological conditions seem to play a key role in reducing the impact of the changes limiting the flow of blood. Neovascularization as a response to ischemia induces sprouting and expansion of the endothelium to repair and grow the vessels of the circulatory system. Neovascularization consists of three different biological processes: vasculogenesis, angiogenesis, and arteriogenesis. Both molecular and environmental factors that may affect the process of development and growth of blood vessels were analyzed. Particular attention was paid to the changes taking place during LEAD. It is important to consider the molecular mechanisms underpinning vessel growth. These mechanisms will also be examined in the context of diseases commonly affecting blood vessel function, or those treatable in part by manipulation of angiogenesis. Furthermore, it may be possible to induce the process of blood vessel development and growth to treat peripheral vascular disease and wound healing. Reactive oxygen species (ROS) play an important role in regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. With regard to the repair processes taking place during diseases such as LEAD, prospective therapeutic methods have been described that could significantly improve the treatment of vessel diseases in the future. Summarizing, regenerative medicine holds the potential to transform the therapeutic methods in heart and vessel diseases treatment. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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30 pages, 2950 KiB  
Review
Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS
by Yunna Lee and Eunok Im
Antioxidants 2021, 10(3), 377; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10030377 - 03 Mar 2021
Cited by 22 | Viewed by 3393
Abstract
Cardiovascular diseases (CVDs) are the most common cause of morbidity and mortality worldwide. The potential benefits of natural antioxidants derived from supplemental nutrients against CVDs are well known. Remarkably, natural antioxidants exert cardioprotective effects by reducing oxidative stress, increasing vasodilation, and normalizing endothelial [...] Read more.
Cardiovascular diseases (CVDs) are the most common cause of morbidity and mortality worldwide. The potential benefits of natural antioxidants derived from supplemental nutrients against CVDs are well known. Remarkably, natural antioxidants exert cardioprotective effects by reducing oxidative stress, increasing vasodilation, and normalizing endothelial dysfunction. Recently, considerable evidence has highlighted an important role played by the synergistic interaction between endothelial nitric oxide synthase (eNOS) and sirtuin 1 (SIRT1) in the maintenance of endothelial function. To provide a new perspective on the role of natural antioxidants against CVDs, we focused on microRNAs (miRNAs), which are important posttranscriptional modulators in human diseases. Several miRNAs are regulated via the consumption of natural antioxidants and are related to the regulation of oxidative stress by targeting eNOS and/or SIRT1. In this review, we have discussed the specific molecular regulation of eNOS/SIRT1-related endothelial dysfunction and its contribution to CVD pathologies; furthermore, we selected nine different miRNAs that target the expression of eNOS and SIRT1 in CVDs. Additionally, we have summarized the alteration of miRNA expression and regulation of activities of miRNA through natural antioxidant consumption. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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26 pages, 1382 KiB  
Review
Pharmacotherapy against Oxidative Stress in Chronic Kidney Disease: Promising Small Molecule Natural Products Targeting Nrf2-HO-1 Signaling
by Md Jamal Uddin, Ee Hyun Kim, Md. Abdul Hannan and Hunjoo Ha
Antioxidants 2021, 10(2), 258; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10020258 - 07 Feb 2021
Cited by 58 | Viewed by 8869
Abstract
The global burden of chronic kidney disease (CKD) intertwined with cardiovascular disease has become a major health problem. Oxidative stress (OS) plays an important role in the pathophysiology of CKD. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant responsive element (ARE) antioxidant system [...] Read more.
The global burden of chronic kidney disease (CKD) intertwined with cardiovascular disease has become a major health problem. Oxidative stress (OS) plays an important role in the pathophysiology of CKD. The nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant responsive element (ARE) antioxidant system plays a critical role in kidney protection by regulating antioxidants during OS. Heme oxygenase-1 (HO-1), one of the targets of Nrf2-ARE, plays an important role in regulating OS and is protective in a variety of human and animal models of kidney disease. Thus, activation of Nrf2-HO-1 signaling may offer a potential approach to the design of novel therapeutic agents for kidney diseases. In this review, we have discussed the association between OS and the pathogenesis of CKD. We propose Nrf2-HO-1 signaling-mediated cell survival systems be explored as pharmacological targets for the treatment of CKD and have reviewed the literature on the beneficial effects of small molecule natural products that may provide protection against CKD. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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27 pages, 1973 KiB  
Review
Therapeutic Effects of Specialized Pro-Resolving Lipids Mediators on Cardiac Fibrosis via NRF2 Activation
by Gyeoung Jin Kang, Eun Ji Kim and Chang Hoon Lee
Antioxidants 2020, 9(12), 1259; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox9121259 - 10 Dec 2020
Cited by 19 | Viewed by 4173
Abstract
Heart disease is the number one mortality disease in the world. In particular, cardiac fibrosis is considered as a major factor causing myocardial infarction and heart failure. In particular, oxidative stress is a major cause of heart fibrosis. In order to control such [...] Read more.
Heart disease is the number one mortality disease in the world. In particular, cardiac fibrosis is considered as a major factor causing myocardial infarction and heart failure. In particular, oxidative stress is a major cause of heart fibrosis. In order to control such oxidative stress, the importance of nuclear factor erythropoietin 2 related factor 2 (NRF2) has recently been highlighted. In this review, we will discuss the activation of NRF2 by docosahexanoic acid (DHA), eicosapentaenoic acid (EPA), and the specialized pro-resolving lipid mediators (SPMs) derived from polyunsaturated lipids, including DHA and EPA. Additionally, we will discuss their effects on cardiac fibrosis via NRF2 activation. Full article
(This article belongs to the Special Issue Natural Antioxidant in Cardiovascular and Cerebrovascular Diseases)
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