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Antioxidants
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Effect of Dietary Antioxidants in Chronic Disease Prevention
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Effect of Dietary Antioxidants in Chronic Disease Prevention

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: 30 October 2024 | Viewed by 12920

Special Issue Editor

Prof. Dr. Baojun Xu

E-Mail Website
Guest Editor
Food Science and Technology Program, Department of Life Sciences, Beijing Normal University-Hong Kong Baptist University United International College, Zhuhai 519087, China
Interests: phytochemicals; natural products; functional foods; human health
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

It is well accepted that a high intake of dietary antioxidants is associated with a decreased chronic disease risk. According to in vitro and in vivo studies, dietary phytochemicals possess therapeutic potential on chronic diseases by modulating different signaling pathways and/or reshaping the gut microbiota. However, the molecular mechanisms behind these activities are not quite clear yet, and further studies are needed to discover the cross-connection in signaling pathway networks between oxidative stress and disease prevention.

In this Special Issue, we will collect and summarize the existing knowledge on disease prevention effects (including anti-tumor activity, anti-obesity, anti-diabetes, anti-inflammatory activity, neuroprotective activity, etc.) of dietary antioxidants. Collections may cover in vitro models, animal models, and human studies. Finally, the underlying molecular mechanisms (such as PI3K/Akt/mTOR, MAPK and NF-кB, etc.) of how these dietary antioxidants regulate their health-promoting effects will be discussed.

Special note: If the dietary antioxidants in a manuscript are mixture compounds, the characterization of the active chemicals in the natural compound should be included using analytical methodologies, such as HPLC, MS, LC–MS, HPLC–MS, and NMR.

Prof. Dr. Baojun Xu
Guest Editor

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

  • dietary antioxidants
  • chronic diseases
  • molecular mechanisms
  • oxidative stress
  • reactive oxygen species
  • inflammation
  • signaling pathways

Published Papers (5 papers)

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Research

16 pages, 28380 KiB  
Article
Protective Effect of Polyphenols Purified from Mallotus oblongfolius on Ethanol-Induced Gastric Mucosal Injury by Regulating Nrf2 and MAPKs Pathways
by Shasha Yu, Zhouwei Duan, Peng Li, Shiping Wang, Lijun Guo, Guanghua Xia and Hui Xie
Antioxidants 2022, 11(12), 2452; https://doi.org/10.3390/antiox11122452 - 12 Dec 2022
Cited by 3 | Viewed by 1280
Abstract
Mallotus oblongifolius (MO), which is rich in polyphenols, is a characteristic tea resource with medicinal value. In this study, a total of 45 polyphenolic components of MO, including narirutin, isoquercitrin, rutin and digallic acid, were identified by UPLC-Q-TOF/MS analysis. In addition, the gastroprotective [...] Read more.
Mallotus oblongifolius (MO), which is rich in polyphenols, is a characteristic tea resource with medicinal value. In this study, a total of 45 polyphenolic components of MO, including narirutin, isoquercitrin, rutin and digallic acid, were identified by UPLC-Q-TOF/MS analysis. In addition, the gastroprotective effect of Mallotus oblongifolius polyphenols (MOP) on ethanol-induced gastric mucosal injury in rats was investigated. The rats received anhydrous ethanol after continuous gavage of MOP or lansoprazole for one week. In addition, the macro- and micro-damage induced by ethanol in the gastric tissue was significantly reduced after MOP pretreatment for one week. Further analysis showed that MOP prevented ethanol-induced acute gastric mucosal injury by increasing the expression of antioxidant enzymes (SOD, CAT, GSH-Px) and decreasing the expression of reactive oxygen species (ROS), lipid oxidation product (MDA) and myeloperoxidase (MPO). Meanwhile, MOP inhibited the phosphorylation of p38/ERK/JNK and promoted the activation of the Nrf2 pathway. These results suggested that MOP may be a promising therapeutic target for the prevention of ethanol-induced gastric mucosal injury by improving oxidative stress, inhibiting the p38/ERK/JNK signaling pathways and activating Nrf2 expression. Full article
(This article belongs to the Special Issue Effect of Dietary Antioxidants in Chronic Disease Prevention)
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15 pages, 3347 KiB  
Article
Quercus acuta Thunb. Suppresses LPS-Induced Neuroinflammation in BV2 Microglial Cells via Regulating MAPK/NF-κB and Nrf2/HO-1 Pathway
by Jae Kwang Kim, Hye Jin Yang and Younghoon Go
Antioxidants 2022, 11(10), 1851; https://doi.org/10.3390/antiox11101851 - 20 Sep 2022
Cited by 4 | Viewed by 1753
Abstract
Microglial activation-mediated neuroinflammation is associated with the pathogenesis of neurodegenerative disorders. Therefore, the management of microglial cell activation and their inflammatory response is an important therapeutic approach for preventing neurodegenerative diseases. Quercus acuta Thunb. (QA) (Fagaceae) is a tree found in [...] Read more.
Microglial activation-mediated neuroinflammation is associated with the pathogenesis of neurodegenerative disorders. Therefore, the management of microglial cell activation and their inflammatory response is an important therapeutic approach for preventing neurodegenerative diseases. Quercus acuta Thunb. (QA) (Fagaceae) is a tree found in Korea, China, and Japan. The current study investigated the anti-neuroinflammatory effects of QA and its mechanism of action in lipopolysaccharide (LPS)-stimulated BV2 microglial cells. Pretreatment with a methanol extract of dried QA stems (QAE) inhibited the production of nitric oxide and proinflammatory cytokines and decreased the expression of inducible nitric oxide synthase, cyclooxygenase-2 in LPS-stimulated BV2 microglial cells. Furthermore, it inhibited the phosphorylation and degradation of inhibitory κBα and decreased the nuclear translocation and phosphorylation of nuclear factor-κB (NF-κB). Moreover, QAE inhibited the phosphorylation of extracellular signal-regulated kinase, p38 and c-Jun N-terminal kinase, which is known as mitogen-activated protein kinase (MAPK). Additionally, QAE treatment increased heme oxygenase-1 (HO-1) expression by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling, thereby ameliorating LPS-induced intracellular hydrogen peroxide production. Finally, it was found that catechin and taxifolin, two phytochemicals of QAE, also reduced the expression of inflammatory mediators. These findings suggest that QA is beneficial for preventing microglia-mediated neuroinflammatory response through the inhibition of NF-κB, MAPK and the activation of Nrf2/HO-1 signaling pathways. Full article
(This article belongs to the Special Issue Effect of Dietary Antioxidants in Chronic Disease Prevention)
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10 pages, 1696 KiB  
Article
β-Carotene Increases Activity of Cytochrome P450 2E1 during Ethanol Consumption
by Cristian Sandoval, Luciana Mella, Karina Godoy, Khosrow Adeli and Jorge Farías
Antioxidants 2022, 11(5), 1033; https://doi.org/10.3390/antiox11051033 - 23 May 2022
Cited by 7 | Viewed by 2221
Abstract
One of the key routes through which ethanol induces oxidative stress appears to be the activation of cytochrome P450 2E1 at different levels of ethanol intake. Our aim was to determine if oral β-carotene intake had an antioxidant effect on CYP2E1 gene expression [...] Read more.
One of the key routes through which ethanol induces oxidative stress appears to be the activation of cytochrome P450 2E1 at different levels of ethanol intake. Our aim was to determine if oral β-carotene intake had an antioxidant effect on CYP2E1 gene expression in mice that had previously consumed ethanol. C57BL/6 mice were used and distributed into: control (C), low-dose alcohol (LA), moderate-dose alcohol (MA), β-carotene (B), low-dose alcohol+β-carotene (LA + B), and moderate-dose alcohol+β-carotene (MA + B). Animals were euthanized at the end of the experiment, and liver tissue was taken from each one. CYP2E1 was measured using qPCR to detect liver damage. The relative expression level of each RNA was estimated using the comparative threshold cycle (Ct) technique (2−ΔΔCT method) by averaging the Ct values from three replicates. The LA+B (2267 ± 0.707) and MA+B (2.307 ± 0.384) groups had the highest CYP2E1 fold change values. On the other hand, the C (1.053 ± 0.292) and LA (1.240 ± 0.163) groups had the lowest levels. These results suggest that ethanol feeding produced a fold increase in CYP2E1 protein in mice as compared to the control group. Increased CYP2E1 activity was found to support the hypothesis that β-carotene might be dangerous during ethanol exposure in animal models. Our findings imply that β-carotene can increase the hepatic damage caused by low and high doses of alcohol. Therefore, the quantity of alcohol ingested, the exposure period, the regulatory mechanisms of alcoholic liver damage, and the signaling pathways involved in the consumption of both alcohol and antioxidant must all be considered. Full article
(This article belongs to the Special Issue Effect of Dietary Antioxidants in Chronic Disease Prevention)
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16 pages, 3271 KiB  
Article
Menthae Herba Attenuates Neuroinflammation by Regulating CREB/Nrf2/HO-1 Pathway in BV2 Microglial Cells
by Yeo Jin Park, Hye Jin Yang, Wei Li, You-Chang Oh and Younghoon Go
Antioxidants 2022, 11(4), 649; https://doi.org/10.3390/antiox11040649 - 28 Mar 2022
Cited by 10 | Viewed by 3036
Abstract
Chronic inflammation and oxidative stress cause microglia to be abnormally activated in the brain, resulting in neurodegenerative diseases such as Alzheimer’s disease (AD). Menthae Herba (MH) has been widely used as a medicinal plant with antimicrobial, anti-inflammatory, and antioxidant properties. In this study, [...] Read more.
Chronic inflammation and oxidative stress cause microglia to be abnormally activated in the brain, resulting in neurodegenerative diseases such as Alzheimer’s disease (AD). Menthae Herba (MH) has been widely used as a medicinal plant with antimicrobial, anti-inflammatory, and antioxidant properties. In this study, we sought to evaluate the effects of MH on the inflammatory response and possible molecular mechanisms in microglia stimulated with lipopolysaccharide (LPS). Transcriptional and translational expression levels of the proinflammatory factors were measured using ELISA, RT-qPCR, and Western blot analysis. MH extract inhibited the production of proinflammatory enzymes and mediators nitric oxide (NO), NO synthase, cyclooxygenase-2, tumor necrosis factor-α, and interleukin-6 in LPS-stimulated cells. Our molecular mechanism study showed that MH inhibited the production of reactive oxygen species (ROS) and the phosphorylation of mitogen-activated protein kinase and nuclear factor (NF)-κB. In contrast, MH activated HO-1 and its transcriptional factors, cAMP response element-binding protein (CREB), and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways. Thus, MH reduces ROS and NF-κB-mediated inflammatory signaling and induces CREB/Nrf2/HO-1-related antioxidant signaling in microglia. Together, these results may provide specific prospects for the therapeutic use of MH in the context of neuroinflammatory diseases, including AD. Full article
(This article belongs to the Special Issue Effect of Dietary Antioxidants in Chronic Disease Prevention)
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11 pages, 2693 KiB  
Article
Synergistic Anti-Inflammatory Effects of Lipophilic Grape Seed Proanthocyanidin and Camellia Oil Combination in LPS-Stimulated RAW264.7 Cells
by Linli Zhang, Juan Chen, Ruihong Liang, Chengmei Liu, Mingshun Chen and Jun Chen
Antioxidants 2022, 11(2), 289; https://doi.org/10.3390/antiox11020289 - 31 Jan 2022
Cited by 14 | Viewed by 3025
Abstract
Combination drug therapy has become an effective strategy to control inflammation. Lipophilic grape seed proanthocyanidin (LGSP) and camellia oil (CO) have been independently investigated to show anti-inflammatory effects, but their synergistic anti-inflammatory effects are unknown. The aim of this study was to investigate [...] Read more.
Combination drug therapy has become an effective strategy to control inflammation. Lipophilic grape seed proanthocyanidin (LGSP) and camellia oil (CO) have been independently investigated to show anti-inflammatory effects, but their synergistic anti-inflammatory effects are unknown. The aim of this study was to investigate the synergistic anti-inflammatory effects of LGSP and CO. The anti-inflammatory activity of LGSP and CO individual or in combination on RAW264.7 cells was detected by MTT assay, Griess reagent, RT-PCR, 2′,7′-dichlorfluoroescein diacetate and Western blot analysis. The combined treatment of LGSP with CO (20 μg/mL and 1 mg/mL) synergistically suppressed the production of NO, TNF-α, IL-6 and ROS. Further studies showed that the synergistic effect was attributed to their suppression of the activation of NF-κB and MAPK signaling pathways. Overall, our findings demonstrate the potential synergistic effect between LGSP and CO in LPS-induced inflammation. Full article
(This article belongs to the Special Issue Effect of Dietary Antioxidants in Chronic Disease Prevention)
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