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Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases

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A special issue of Molecules (ISSN 1420-3049). This special issue belongs to the section "Natural Products Chemistry".

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 46329

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Special Issue Editors

Dr. Raluca Maria Pop

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Department of Pharmacology, Toxicology and Clinical Pharmacology, University of Medicine and Pharmacy Iuliu Hatieganu Cluj-Napoca, Victor Babes, 8, 400000 Cluj-Napoca, Romania
Interests: spectroscopy; chromatography; mass spectrometry; plant bioactive compounds; antioxidant activity; oxidative stress and inflammation; cardiovascular diseases
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Dr. Ada Popolo

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Department of Pharmacy, University of Salerno, 84084 Fisciano, SA, Italy
Interests: cardiovascular toxicology; calcium homeostasis; clinical pharmacology; oxidative stress; inflammation
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Dr. Stefan Cristian Vesa

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Department of Pharmacology, Toxicology and Clinical Pharmacology, University of Medicine and Pharmacy Iuliu Hatieganu Cluj-Napoca, Cluj-Napoca, Romania
Interests: ultrasound imaging; ultrasonography; heart failure; internal medicine; cardiovascular disease; metabolic syndrome; pharmacology; cardiology; pharmacodynamics; atherosclerosis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is already known that prolonged chronic inflammation influences the development of several chronic diseases such as cancer, cardiovascular, respiratory, and metabolic diseases, Alzheimer’s disease, arthrosis and others. During chronic inflammation, mediators such as cytokines, chemokines, oxidants, eicosanoids or lytic enzymes are released from immune cells, being actively involved in the progression and development of inflammatory processes. The transcription factor NF-κB has a pivotal role since it regulates pro-inflammatory gene expression, including the genes encoding cytokine and chemokine production. An incorrect NF-kB regulation will induce prolonged inflammation, acting as a central transcription factor, which is highly important in chronic inflammatory disease development. Additionally, cyclooxygenase (COX) and lipoxygenase (LOX) are some of the principal enzymes that mediate the inflammation process. The production of prostaglandins (PGEs) and thromboxane is dependent on arachidonic acid COX catalyzation, while the production of leukotrienes (LTs) is dependent on LOX activity. Furthermore, during normal inflammatory metabolic processes, neutrophils and macrophages produce reactive oxygen species (ROS) such as hydrogen peroxide (H₂O₂), hypochlorous acid (HOCl-), superoxide radical (O2•-), peroxynitrite (ONOO) and nitric oxide (NO). During chronic inflammation, prolonged ROS production can lead to oxidative stress, which is considered central in the progression of inflammatory diseases. An increased ROS production in the absence of specific protective mechanisms will initiate intracellular signalling of specific proinflammatory genes expression, which will eventually lead to chronic inflammation.

Knowing that both inflammation and oxidative stress processes are strongly linked and involved in the initiation and maintenance of many pathological conditions, their prevention and control must be the target in obtaining efficient management of chronic diseases.

In this regard, alternative therapies involving natural bioactive molecules that are able to specifically target the oxidative stress and inflammation processes could provide efficacy along with a good safety profile. That is why they are on the research pipe of many scientists around the world. Thus, bioactive molecules could be considered an ideal approach to the limitations of classical therapy. This Special Issue will focus on phytochemical antioxidants and anti-inflammatory activities, as well as their role in the treatment and management of related diseases.

Dr. Ing. Raluca Maria Pop
Dr. Ada Popolo
Dr. Stefan Cristian Vesa
Guest Editors

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Keywords

Cardiovascular diseases
Bioactive molecules
Oxidative stress
Inflammation
Natural products

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Published Papers (11 papers)

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16 pages, 2126 KiB

Open AccessArticle

A Novel Distachionate from Breynia distachia Treats Inflammations by Modulating COX-2 and Inflammatory Cytokines in Rat Liver Tissue

by Malik Saadullah, Muhammad Asif, Arshad Farid, Faiza Naseem, Sheikh Abdur Rashid, Shakira Ghazanfar, Muhammad Muzammal, Sohail Ahmad, Yousef A. Bin Jardan, Huda Alshaya, Muhammad Hamzah Saleem, Shafaqat Ali, Charles Oluwaseun Adetunji and Sania Arif

Molecules 2022, 27(8), 2596; https://doi.org/10.3390/molecules27082596 - 18 Apr 2022

Cited by 22 | Viewed by 2564

Abstract

Breynia distachia is a plant of genus Breynia belonging to family Phyllanthaceae. This study was conducted to isolate and examine the anti-inflammatory attributes of the roots of Breynia distachia. Methanol extract from roots were prepared by simple maceration. For phytochemical studies, isolation, purification, structure elucidation, metal analysis, total phenolic content, and solubility test were done by chromatographic and spectroscopic techniques. Anti-inflammatory activity was evaluated by cotton pallet edema model and carrageenan paw edema model, and antioxidant potential was evaluated by DPPH, FRAP, and ABTS antioxidants assays. Metal analysis of BD.Me revealed the presence of Na > Mg > K > Mn > Fe = Zn in respective order. Four phytochemicals such as gallic acid, quercetin, sinapic acid, and p-coumaric acid are found in Breynia distachia. Quercetin is present in relatively larger quantity, and shows antioxidant activity by reducing the ferric iron to ferrous iron. Novel distachionate shows high antioxidant activity in ABTS assay by reducing reactive oxygen species. Quantitative or qualitative analysis performed by HPLC indicates the ascending peaks or presence of secondary products (metabolites) respectively. Histopathology analysis of liver, spleen, heart, and kidney was done, revealing mild inflammations in spleen and liver, and no cytotoxicity in heart and kidney. Oral administration of BD.Me and ditachionate significantly inhibits the carrageenan and cotton pellet-induced paw edema in 1st and 2nd h with (ns = p > 0.05) than control. After 3rd, 4th, 5th, and 6th h, BD.Me and ditachionate showed inhibition of paw edema in a highly significant (*** = p < 0.001) manner as compared to control. In cotton-pellet edema model, distachionate shows a %inhibition of 57.3% at a dose level of 5 mg/kg. Docking values obtained from distachionate-COX-2 complex suggest a potent inhibitor evaluated for this protein. The distachionate shows effective anti-inflammatory activity. Methanol extracts of roots showed significant lipoxygenase inhibitory activity by IC₅₀ values of 155.7 ± 0.55 and 132.9 ± 0.33 μg/mL. Data from various in vitro and in vivo models suggest that novel distachionate isolated from Breynia distachia shows strong antioxidant and anti-inflammatory activities; it should be further studied for the exploration of its medicinal potential. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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12 pages, 2192 KiB

Open AccessArticle

Piceatannol Protects Brain Endothelial Cell Line (bEnd.3) against Lipopolysaccharide-Induced Inflammation and Oxidative Stress

by Yan Zhou, Haroon Khan, Maggie Pui Man Hoi and Wai San Cheang

Molecules 2022, 27(4), 1206; https://doi.org/10.3390/molecules27041206 - 11 Feb 2022

Cited by 14 | Viewed by 3397

Abstract

Dysfunction of the blood–brain barrier (BBB) is involved in the pathogenesis of many cerebral diseases. Oxidative stress and inflammation are contributing factors for BBB injury. Piceatannol, a natural ingredient found in various plants, such as grapes, white tea, and passion fruit, plays an important role in antioxidant and anti-inflammatory responses. In this study, we examined the protective effects of piceatannol on lipopolysaccharide (LPS) insult in mouse brain endothelial cell line (bEnd.3) cells and the underlying mechanisms. The results showed that piceatannol mitigated the upregulated expression of adhesion molecules (ICAM-1 and VCAM-1) and iNOS in LPS-treated bEnd.3 cells. Moreover, piceatannol prevented the generation of reactive oxygen species in bEnd.3 cells stimulated with LPS. Mechanism investigations suggested that piceatannol inhibited NF-κB and MAPK activation. Taken together, these observations suggest that piceatannol reduces inflammation and oxidative stress through inactivating the NF-κB and MAPK signaling pathways on cerebral endothelial cells in vitro. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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10 pages, 3967 KiB

Open AccessArticle

The Effect of Homocysteine on the Secretion of Il-1β, Il-6, Il-10, Il-12 and RANTES by Peripheral Blood Mononuclear Cells—An In Vitro Study

by Magdalena Borowska, Hanna Winiarska, Marzena Dworacka, Anna Wesołowska, Grzegorz Dworacki and Przemysław Łukasz Mikołajczak

Molecules 2021, 26(21), 6671; https://doi.org/10.3390/molecules26216671 - 4 Nov 2021

Cited by 6 | Viewed by 2352

Abstract

The contemporary theory of the inflammatory-immunological pathomechanism of atherosclerosis includes the participation of interleukin-1β (Il), Il-6, Il-10, Il-12, RANTES, and homocysteine in this process. The knowledge on the direct effect of hyperhomocysteinemia on inflammatory-state-related atherosclerosis is rather scarce. Our study is the first to account for the effects of homocysteine on the secretion of Il-10 and RANTES in vitro conditions. For this purpose, human mitogen-stimulated peripheral blood mononuclear cells (PBMNCs) were cultured in vitro and exposed to homocysteine at high concentrations. Subsequently, the concentrations of cytokines were assayed in the cell culture supernatant using flow cytofluorimetry. It has been shown that, in the presence of homocysteine, the secretion of IL-1, IL-6 and RANTES by PBMNCs was increased, whereas IL-10 concentration was significantly lower than that of the supernatant derived from a mitogen-stimulated cell culture without homocysteine. The secretion of Il-12 by PBMNCs exposed exclusively to mitogen, did not differ from homologous cells also treated with homocysteine. Therefore, in our opinion, high-concentration homocysteine affects the progression of atherosclerosis by increasing the secretion of proinflammatory cytokines secreted by PBMNCs, such as Il-1β, Il-6, RANTES, and by attenuating the secretion of Il-10. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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16 pages, 5210 KiB

Open AccessArticle

Differential Effects of Ruminant and Industrial 18-Carbon trans-Monounsaturated Fatty Acids (trans Vaccenic and Elaidic) on the Inflammatory Responses of an Endothelial Cell Line

by Carina A. Valenzuela, Ella J. Baker, Camila O. De Souza, Elizabeth A. Miles and Philip C. Calder

Molecules 2021, 26(19), 5834; https://doi.org/10.3390/molecules26195834 - 26 Sep 2021

Cited by 8 | Viewed by 2327

Abstract

Endothelial dysfunction and inflammation are recognised factors in the development of atherosclerosis. Evidence suggests that intake of industrial trans fatty acids (TFAs) promotes endothelial dysfunction, while ruminant TFAs may have the opposite effect. The aim of this study was to compare the effects of elaidic acid (EA (18:1n-9t); an industrially produced TFA) and trans vaccenic acid (TVA (18:1n-7t); a natural TFA found in ruminant milk and meat) on inflammatory responses of endothelial cells (ECs). ECs (EA.hy926 cells) were cultured under standard conditions and exposed to TFAs (1 to 50 μM) for 48 h. Then, the cells were cultured for a further 6 or 24 h with tumour necrosis factor alpha (TNF-α, 1 ng/mL) as an inflammatory stimulant. ECs remained viable after treatments. TFAs were incorporated into ECs in a dose-dependent manner. Preincubation with EA (50 µM) increased production of MCP-1, RANTES, and IL-8 in response to TNF-α, while preincubation with TVA (1 µM) decreased production of ICAM-1 and RANTES in response to TNF-α. Preincubation with EA (50 µM) upregulated toll-like receptor 4 and cyclooxygenase 2 gene expression in response to TNF-α. In contrast, preincubation with TVA (1 µM) downregulated TNF-α induced nuclear factor kappa B subunit 1 gene expression. Preincubation of ECs with EA (50 µM) increased THP-1 monocyte adhesion. In contrast, preincubation of ECs with TVA (1 µM) reduced THP-1 monocyte adhesion, while preincubation of ECs with TVA (50 µM) decreased the level of surface expression of ICAM-1 seen following TNF-α stimulation. The results suggest that TVA has some anti-inflammatory properties, while EA enhances the response to an inflammatory stimulus. These findings suggest differential effects induced by the TFAs tested, fitting with the idea that industrial TFAs and ruminant TFAs can have different and perhaps opposing biological actions in an inflammatory context. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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10 pages, 1984 KiB

Open AccessArticle

Coptisine Attenuates Diabetes—Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress

by Yan Zhou, Chunxiu Zhou, Xutao Zhang, Chi Teng Vong, Yitao Wang and Wai San Cheang

Molecules 2021, 26(14), 4210; https://doi.org/10.3390/molecules26144210 - 11 Jul 2021

Cited by 17 | Viewed by 2651

Abstract

Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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17 pages, 3049 KiB

Open AccessArticle

Identification of Human Kinin-Forming Enzyme Inhibitors from Medicinal Herbs

by Hassan Madkhali, Amer Tarawneh, Zulfiqar Ali, Hoang V. Le, Stephen J. Cutler, Ikhlas A. Khan and Zia Shariat-Madar

Molecules 2021, 26(14), 4126; https://doi.org/10.3390/molecules26144126 - 7 Jul 2021

Cited by 2 | Viewed by 2754

Abstract

The goal of this study was to assess the pharmacological effects of black tea (Camellia sinensis var. assamica) water extract on human kinin-forming enzymes in vitro. Tea is a highly consumed beverage in the world. Factor XII (FXII, Hageman factor)-independent- and -dependent activation of prekallikrein to kallikrein leads to the liberation of bradykinin (BK) from high-molecular-weight kininogen (HK). The excessive BK production causes vascular endothelial and nonvascular smooth muscle cell permeability, leading to angioedema. The prevalence of angiotensin-converting enzyme inhibitor (ACEI)-induced angioedema appears to be through BK. Both histamine and BK are potent inflammatory mediators. However, the treatments for histamine-mediated angioedema are unsuitable for BK-mediated angioedema. We hypothesized that long-term consumption of tea would reduce bradykinin-dependent processes within the systemic and pulmonary vasculature, independent of the anti-inflammatory actions of polyphenols. A purified fraction of the black tea water extract inhibited both kallikrein and activated FXII. The black tea water extracts inhibited factor XII-induced cell migration and inhibited the production of kallikrein on the endothelial cell line. We compared the inhibitory effects of the black tea water extract and twenty-three well-known anti-inflammatory medicinal herbs, in inhibiting both kallikrein and FXII. Surprisingly, arjunglucoside II specifically inhibited the activated factor XII (FXIIa), but not the kallikrein and the activated factor XI. Taken together, the black tea water extract exerts its anti-inflammatory effects, in part, by inhibiting kallikrein and activated FXII, which are part of the plasma kallikrein–kinin system (KKS), and by decreasing BK production. The inhibition of kallikrein and activated FXII represents a unique polyphenol-independent anti-inflammatory mechanism of action for the black tea. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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18 pages, 2075 KiB

Open AccessArticle

Comparative Protective Effect of Nigella sativa Oil and Vitis vinifera Seed Oil in an Experimental Model of Isoproterenol-Induced Acute Myocardial Ischemia in Rats

by Ioana Corina Bocsan, Raluca Maria Pop, Octavia Sabin, Elias Sarkandy, Paul-Mihai Boarescu, Ştefan Horia Roşian, Poliana Mihaela Leru, Veronica Sanda Chedea, Sonia Ancuța Socaci and Anca Dana Buzoianu

Molecules 2021, 26(11), 3221; https://doi.org/10.3390/molecules26113221 - 27 May 2021

Cited by 17 | Viewed by 3597

Abstract

The study’s aim was to characterize the composition of Nigella sativa seed (NSO) and grape seed (GSO) oils, and to evaluate their cardioprotective and anti-inflammatory effect on isoproterenol (ISO)-induced ischemia in rats. Materials and Methods: NSO and GSO supplements were physicochemically characterized. Liquid chromatography–mass spectrometry (HPLC-MS), Fourier-transform infrared spectroscopy (FTIR), and gas chromatography–mass spectrometry (GC-MS) analyses were used to determine the phytochemical composition in the oils. Total polyphenol content (TPC) and in vitro antioxidant activity were also determined. Pretreatment with 4 mL/kg/day NSO or GSO was administered to rats for 14 days. The experimental ischemia was induced by a single administration of ISO 45 mg/kg after 14 days. An electrocardiogram (ECG) was performed initially and 24 h after ISO. Biological evaluation was done at the end of experiment. Results: The HPLC-MS, GC-MS, and FTIR analyses showed that both NSO and GSO are important sources of bioactive compounds, especially catechin and phenolic acids in GSO, while NSO was enriched in flavonoids and thymol derivatives. Pretreatment with GSO and NSO significantly reduced ventricular conduction, prevented the cardiotoxic effect of ISO in ventricular myocardium, and reduced the level of proinflammatory cytokines and CK-Mb. Conclusion: Both NSO and GSO were shown to have an anti-inflammatory and cardioprotective effect in ISO-induced ischemia. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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19 pages, 3437 KiB

Open AccessArticle

Divergent and Overlapping Roles for Selected Phytochemicals in the Regulation of Pathological Cardiac Hypertrophy

by Levi Evans, Yiqui Shen, Abigail Bender, Leah E. Burnett, Musheng Li, Justine S. Habibian, Tong Zhou and Bradley S. Ferguson

Molecules 2021, 26(5), 1210; https://doi.org/10.3390/molecules26051210 - 24 Feb 2021

Cited by 9 | Viewed by 3004

Abstract

Plant-based foods, like fruits, vegetables, whole grains, legumes, nuts, seeds and other foodstuffs, have been deemed as heart healthy. The chemicals within these plant-based foods, i.e., phytochemicals, are credited with protecting the heart. However, the mechanistic actions of phytochemicals, which prevent clinical endpoints, such as pathological cardiac hypertrophy, are still being elucidated. We sought to characterize the overlapping and divergent mechanisms by which 18 selected phytochemicals prevent phenylephrine- and phorbol 12-myristate 13-acetate-mediated cardiomyocyte enlargement. Of the tested 18 compounds, six attenuated PE- and PMA-mediated enlargement of neonatal rat ventricular myocytes. Cell viability assays showed that apigenin, baicalein, berberine hydrochloride, emodin, luteolin and quercetin dihydrate did not reduce cell size through cytotoxicity. Four of the six phytochemicals, apigenin, baicalein, berberine hydrochloride and emodin, robustly inhibited stress-induced hypertrophy and were analyzed further against intracellular signaling and genome-wide changes in mRNA expression. The four phytochemicals differentially regulated mitogen-activated protein kinases and protein kinase D. RNA-sequencing further showed divergence in gene regulation, while pathway analysis demonstrated overlap in the regulation of inflammatory pathways. Combined, this study provided a comprehensive analysis of cardioprotective phytochemicals. These data highlight two defining observations: (1) that these compounds predominantly target divergent gene pathways within cardiac myocytes and (2) that regulation of overlapping signaling and gene pathways may be of particular importance for the anti-hypertrophic actions of these phytochemicals. Despite these new findings, future works investigating rodent models of heart failure are still needed to understand the roles for these compounds in the heart. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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18 pages, 1609 KiB

Open AccessArticle

Evaluation of the Antioxidant Activity of Nigella sativa L. and Allium ursinum Extracts in a Cellular Model of Doxorubicin-Induced Cardiotoxicity

by Raluca Maria Pop, Ioana Corina Bocsan, Anca Dana Buzoianu, Veronica Sanda Chedea, Sonia Ancuța Socaci, Michela Pecoraro and Ada Popolo

Molecules 2020, 25(22), 5259; https://doi.org/10.3390/molecules25225259 - 11 Nov 2020

Cited by 18 | Viewed by 3866

Abstract

Natural products black cumin—Nigella sativa (N. sativa) and wild garlic—Allium ursinum (AU) are known for their potential role in reducing cardiovascular risk factors, including antracycline chemotherapy. Therefore, this study investigates the effect of N. sativa and AU water and methanolic extracts in a cellular model of doxorubicin (doxo)-induced cardiotoxicity. The extracts were characterized using Ultraviolet-visible (UV-VIS) spectroscopy, Fourier-transform infrared (FT-IR) spectroscopy, Liquid Chromatography coupled with Mass Spectrometry (LC-MS) and Gas Chromatography coupled with Mass Spectrometry (GC-MS) techniques. Antioxidant activity was evaluated on H9c2 cells. Cytosolic and mitochondrial reactive oxygen species (ROS) release was evaluated using 2′,7′-dichlorofluorescin-diacetate (DHCF-DA) and mitochondria-targeted superoxide indicator (MitoSOX red), respectively. Mitochondrial membrane depolarization was evaluated by flow cytometry. LC-MS analysis identified 12 and 10 phenolic compounds in NSS and AU extracts, respectively, with flavonols as predominant compounds. FT-IR analysis identified the presence of carbohydrates, amino acids and lipids in both plants. GC-MS identified the sulfur compounds in the AU water extract. N. sativa seeds (NSS) methanolic extract had the highest antioxidant activity reducing both intracellular and mitochondrial ROS release. All extracts (excepting AU methanolic extract) preserved H9c2 cells viability. None of the investigated plants affected the mitochondrial membrane depolarization. N. sativa and AU are important sources of bioactive compounds with increased antioxidant activities, requiring different extraction solvents to obtain the pharmacological effects. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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Review

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18 pages, 297 KiB

Open AccessReview

The Effects of Flavonoids in Cardiovascular Diseases

by Lorena Ciumărnean, Mircea Vasile Milaciu, Octavia Runcan, Ștefan Cristian Vesa, Andreea Liana Răchișan, Vasile Negrean, Mirela-Georgiana Perné, Valer Ioan Donca, Teodora-Gabriela Alexescu, Ioana Para and Gabriela Dogaru

Molecules 2020, 25(18), 4320; https://doi.org/10.3390/molecules25184320 - 21 Sep 2020

Cited by 245 | Viewed by 13863

Abstract

Flavonoids are metabolites of plants and fungus. Flavonoid research has been paid special attention to in recent times after the observation of their beneficial effects on the cardiovascular system. These favorable effects are exerted by flavonoids mainly due to their antioxidant properties, which result from the ability to decrease the oxidation of low-density lipoproteins, thus improving the lipid profiles. The other positive effect exerted on the cardiovascular system is the ability of flavonoids to produce vasodilation and regulate the apoptotic processes in the endothelium. Researchers suggested that these effects, including their anti-inflammatory function, are consequences of flavonoids’ potent antioxidant properties, but recent studies have shown multiple signaling pathways linked to them, thus suggesting that there are more mechanisms involved in the beneficial effect of the flavonoids on the human body. This review aims to present the latest data on the classification of these substances, their main mechanisms of action in the human body, and the beneficial effects on the physiological and pathological status of the cardiovascular system. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

21 pages, 292 KiB

Open AccessReview

The Effect of Vitamin Supplementation on Subclinical Atherosclerosis in Patients without Manifest Cardiovascular Diseases: Never-ending Hope or Underestimated Effect?

by Ovidiu Mitu, Ioana Alexandra Cirneala, Andrada Ioana Lupsan, Mircea Iurciuc, Ivona Mitu, Daniela Cristina Dimitriu, Alexandru Dan Costache, Antoniu Octavian Petris and Irina Iuliana Costache

Molecules 2020, 25(7), 1717; https://doi.org/10.3390/molecules25071717 - 9 Apr 2020

Cited by 16 | Viewed by 3969

Abstract

Micronutrients, especially vitamins, play an important role in the evolution of cardiovascular diseases (CVD). It has been speculated that additional intake of vitamins may reduce the CVD burden by acting on the inflammatory and oxidative response starting from early stages of atherosclerosis, when the vascular impairment might still be reversible or, at least, slowed down. The current review assesses the role of major vitamins on subclinical atherosclerosis process and the potential clinical implications in patients without CVD. We have comprehensively examined the literature data for the major vitamins: A, B group, C, D, and E, respectively. Most data are based on vitamin E, D and C supplementation, while vitamins A and B have been scarcely examined for the subclinical atherosclerosis action. Though the fundamental premise was optimistic, the up-to-date trials with vitamin supplementation revealed divergent results on subclinical atherosclerosis improvement, both in healthy subjects and patients with CVD, while the long-term effect seems minimal. Thus, there are no conclusive data on the prevention and progression of atherosclerosis based on vitamin supplementation. However, given their enormous potential, future trials are certainly needed for a more tailored CVD prevention focusing on early stages as subclinical atherosclerosis. Full article

(This article belongs to the Special Issue Bioactive Molecules Targeting Inflammation and Oxidative Stress Processes in Related Diseases)

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