Dietary Antioxidants and Inflammation-Induced Chronic 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 (31 December 2023) | Viewed by 11935

Special Issue Editors


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Guest Editor
Institute of Vegetable and Flower, Chinese Academy of Agricultural Sciences, Beijing, China
Interests: natural products and chronic disease prevention; food chemistry and nutrition; bioactive lipids in cancer
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China
Interests: phytochemicals; prevention or treatment of chronic diseases; lipid metabolites and cancer
Special Issues, Collections and Topics in MDPI journals

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Guest Editor Assistant
Laboratory of Biochemistry, Wageningen University & Research, Wageningen, The Netherlands
Interests: application of muti-omics in food science; food chemistry and nutrition; glycans in gut microbiota

Special Issue Information

Dear Colleagues,

Inflammation is the basic cause of many chronic diseases, including cardiovascular disease, obesity, diabetes, enteritis, Alzheimer's disease, and cancer. Suppressing or eliminating inflammation in the body is an effective way to prevent or treat chronic diseases. Free radicals can lead to an imbalance in inflammatory homeostasis, which in turn causes excess free radicals, further exacerbating the occurrence and development of inflammatory diseases. Chronic inflammatory processes can lead to the enhancement of oxidative stress and a reduction in the intracellular antioxidant capacity, which further stimulates the activation of inflammatory cells, thus forming a vicious spiral between oxidative stress and the inflammatory response. Dietary antioxidants (e.g., polyphenols, carotenoids, polysaccharides, saponins, vitamins, triterpenoids, etc.) from fruits and vegetables can effectively scavenge free radicals to alleviate inflammatory-stimulated chronic disease through multiple metabolic pathways including the inhibition of oxidative stress, resolution of inflammation, regulation of lipid metabolism/gut microbiota, and activation of immune responses. It is of great interest to excavate natural antioxidants with anti-inflammatory effects from the diet and elucidate the molecular mechanisms for the prevention and treatment of chronic diseases.

The purpose of this Special Issue is to provide a platform for scholars studying the relationship between dietary antioxidants and chronic inflammatory diseases and its related fields. We would like you to submit the high-quality research in the form of original research articles, reviews, or mini-reviews based on but not limited to: the isolation, purification, and structural identification of dietary antioxidants; dietary antioxidants and gut microbiota; dietary antioxidants and cytokine storm; dietary antioxidants and oxidative stress; dietary antioxidants and immune responses; etc.

Prof. Dr. Jianjun Deng
Prof. Dr. Haixia Yang
Guest Editors

Dr. Wenyuan Zhang
Guest Editor Assistant

Manuscript Submission Information

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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 antioxidations
  •  chronic diseases
  •  inflammatory cytokines
  •  structural identification
  •  gut microbiota
  •  oxidative stress
  •  immune responses
  •  lipid metabolism
  •  free radicals

Published Papers (4 papers)

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Research

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20 pages, 72883 KiB  
Article
Astaxanthin Protects against Hyperglycemia-Induced Oxidative and Inflammatory Damage to Bone Marrow and to Bone Marrow-Retained Stem Cells and Restores Normal Hematopoiesis in Streptozotocin-Induced Diabetic Mice
by Govinda Bhattarai, Han-Sol So, Tae-Geum Kim, Thi Thu Trang Kieu, Yeon-Woo Kim, Ku-Ri Yang, Jeong-Chae Lee, Sung-Ho Kook and Young-Mi Jeon
Antioxidants 2022, 11(12), 2321; https://doi.org/10.3390/antiox11122321 - 23 Nov 2022
Viewed by 1550
Abstract
Hyperglycemia has various adverse health effects, some of which are due to chronic oxidative and inflammatory impairment of bone marrow (BM), hematopoietic stem cells (HSCs), and mesenchymal stem cells (MSCs). Astaxanthin (ASTX) has been shown to ameliorate hyperglycemia-associated systemic complications and acute mortality, [...] Read more.
Hyperglycemia has various adverse health effects, some of which are due to chronic oxidative and inflammatory impairment of bone marrow (BM), hematopoietic stem cells (HSCs), and mesenchymal stem cells (MSCs). Astaxanthin (ASTX) has been shown to ameliorate hyperglycemia-associated systemic complications and acute mortality, and this effect is partially associated with restoration of normal hematopoiesis. Here, the effects of ASTX on diabetes-induced complications in BM and BM stem cells were investigated, and the underlying molecular mechanisms were elucidated. Ten-week-old C57BL/6 mice received a single intraperitoneal injection of streptozotocin (STZ; 150 mg/kg) in combination with oral gavage of ASTX (12.5 mg/kg) for 30 or 60 consecutive days. Supplemental ASTX ameliorated acute mortality and restored the STZ-impaired bone mass accrual and BM microenvironment in STZ-injected mice. Oral gavage of ASTX suppressed osteoclast formation in the BM of STZ-injected mice. Specifically, supplementation with ASTX inhibited oxidative stress and senescence induction of BM HSCs and MSCs and ameliorated hematopoietic disorders in STZ-injected mice. These effects of ASTX were associated with BM restoration of angiopoietin 1, stromal cell-derived factor 1, β-catenin, and Nrf2. Long-term ASTX gavage also recovered the STZ-induced dysfunction in migration, colony formation, and mineralization of BM-derived stromal cells. Further, a direct addition of ASTX exhibited direct and dose-dependent inhibition of osteoclastic activation without cytotoxic effects. Collectively, these results indicate that ASTX protects against diabetes-induced damage in the BM microenvironment in BM, HSCs, and MSCs and restores normal hematopoiesis and bone accrual in STZ-injected mice. Full article
(This article belongs to the Special Issue Dietary Antioxidants and Inflammation-Induced Chronic Diseases)
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20 pages, 17853 KiB  
Article
Water Caltrop (Trapa quadrispinosa Roxb.) Husk Improves Oxidative Stress and Postprandial Blood Glucose in Diabetes: Phenolic Profiles, Antioxidant Activities and α-Glycosidase Inhibition of Different Fractions with In Vitro and In Silico Analyses
by Yuanyue Zhang, Shengbao Cai, Shuang Ma, Shuai Zhao, Junjie Yi and Linyan Zhou
Antioxidants 2022, 11(10), 1873; https://doi.org/10.3390/antiox11101873 - 21 Sep 2022
Cited by 8 | Viewed by 1858
Abstract
The aim of this study was to investigate the phenolic profiles, antioxidant activities and α-glycosidase inhibitory activities of three different phenolic fractions from water caltrop (Trapa quadrispinosa Roxb.) husk and to further explore the predominant compounds and their mechanisms on α-glycosidase inhibition [...] Read more.
The aim of this study was to investigate the phenolic profiles, antioxidant activities and α-glycosidase inhibitory activities of three different phenolic fractions from water caltrop (Trapa quadrispinosa Roxb.) husk and to further explore the predominant compounds and their mechanisms on α-glycosidase inhibition by virtual screening and molecular dynamics. A total of 29 substances were identified and quantified in this study. Tannins were the main constituents of water caltrop husk extract. All of the free phenolic (FP), esterified phenolic (EP) and insoluble-bound phenolic (BP) fractions exhibited good antioxidant activities, and the BP had the highest radical scavenging ability with IC50 values of 0.82 ± 0.12 μg/mL (ABTS) and 1.15 ± 0.02 μg/mL (DPPH), respectively (p < 0.05). However, compared with the EP and BP, the FP showed the strongest inhibition towards the α-glycosidase and the IC50 value of FP was 1.43 ± 0.12 μg/mL. The 1,2,6-trigalloylglucose and α-glycosidase complex had better root mean square deviations (RMSD) stability via molecular dynamics simulation study. Results obtained from this study may provide a good potential natural resource for the improvement of oxidative stress injury and blood glucose control in diabetes mellitus, which could expand the use of water caltrop husk and improve its economic value. Full article
(This article belongs to the Special Issue Dietary Antioxidants and Inflammation-Induced Chronic Diseases)
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20 pages, 3997 KiB  
Article
Diosmin and Trolox Have Anti-Arthritic, Anti-Inflammatory and Antioxidant Potencies in Complete Freund’s Adjuvant-Induced Arthritic Male Wistar Rats: Roles of NF-κB, iNOS, Nrf2 and MMPs
by Huda H. Shaaban, Walaa G. Hozayen, Amal K. Khaliefa, Ayman E. El-Kenawy, Tarek M. Ali and Osama M. Ahmed
Antioxidants 2022, 11(9), 1721; https://doi.org/10.3390/antiox11091721 - 30 Aug 2022
Cited by 12 | Viewed by 3012
Abstract
Rheumatoid arthritis (RA) is a chronic, progressive, autoimmune disease caused by a malfunction of the immune system. The aim of this study was to examine the anti-arthritic effects and suggest the mechanisms of actions of diosmin and trolox in male Wistar rats. Complete [...] Read more.
Rheumatoid arthritis (RA) is a chronic, progressive, autoimmune disease caused by a malfunction of the immune system. The aim of this study was to examine the anti-arthritic effects and suggest the mechanisms of actions of diosmin and trolox in male Wistar rats. Complete Freund’s adjuvant (CFA) was used to establish RA in the animals by subcutaneous injection of 100 µL CFA/rat into plantar region of right hind leg in two consecutive days. Diosmin and/or trolox were administered orally at a dosage of 20 mg/kg/day to CFA-induced arthritic rats for 2 weeks. The normal and arthritic control groups were orally given the same equivalent volume of a vehicle (1% carboxymethyl cellulose) in which treatment agents were dissolved. At the end of the experiment, blood samples were collected from the jugular vein for the detection of the total leukocyte count (TLC) and differential leukocyte count (DLC) in blood and the detection of rheumatoid factor (RF), anti-citrullinated protein antibodies (ACPA), tumor necrosis factor-α (TNF-α), interleukin-13 (IL-13), and interleukin-17 (IL-17) levels by enzyme-linked immunosorbent assay (ELISA), as well as markers of oxidative stress and the antioxidant defense system in serum. The right hind ankle regions of three rats from each group were dissected out and fixed in 10% neutral-buffered formalin for histological examination and the other three were kept at −30 °C for Western blot analysis of nuclear factor-kappa B (NF-κB) protein 50 (NF-κB p50), NF-κB p65, inducible nitric oxide synthase (iNOS), nuclear factor erythroid-2-related factor 2 (Nrf2), and matrix metalloproteinase (MMP)-1 (MMP-1), MMP-3, and MMP-9. The CFA injection was deleterious to the ankle joint’s histological architecture, manifesting as infiltration of inflammatory cells into the articular cartilage, hyperplasia of the synovium, and erosion of the cartilage. All these effects were ameliorated by diosmin and/or trolox, with the combined dose being the most effective. The two compounds significantly lowered the elevated serum levels of RF, ACPA, TNF-α, and IL-17, as well as other pro-inflammatory mediators, such as NF-κB p50, NF-κB p65, iNOS, MMP-1, MMP-3 and MMP-9. They also increased the levels of the anti-inflammatory cytokine, IL-13, and the cytoprotective transcription factor Nrf2. The compounds stimulated higher activities of antioxidants, such as glutathione, glutathione-S-transferase, catalase, and superoxide dismutase, and reduced lipid peroxidation in the serum of arthritic rats. In conclusion, diosmin, trolox, and their combination, which was the most potent, exerted anti-arthritic, anti-inflammatory and antioxidant effects by suppressing NF-κB signaling, inhibiting matrix metalloproteinases, and activating Nrf2. Full article
(This article belongs to the Special Issue Dietary Antioxidants and Inflammation-Induced Chronic Diseases)
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Review

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23 pages, 3008 KiB  
Review
Aflatoxin B1 Toxicity and Protective Effects of Curcumin: Molecular Mechanisms and Clinical Implications
by Chongshan Dai, Erjie Tian, Zhihui Hao, Shusheng Tang, Zhanhui Wang, Gaurav Sharma, Haiyang Jiang and Jianzhong Shen
Antioxidants 2022, 11(10), 2031; https://doi.org/10.3390/antiox11102031 - 14 Oct 2022
Cited by 25 | Viewed by 4562
Abstract
One of the most significant classes of mycotoxins, aflatoxins (AFTs), can cause a variety of detrimental outcomes, including cancer, hepatitis, aberrant mutations, and reproductive issues. Among the 21 identified AFTs, aflatoxin B1 (AFB1) is the most harmful to humans and animals. The mechanisms [...] Read more.
One of the most significant classes of mycotoxins, aflatoxins (AFTs), can cause a variety of detrimental outcomes, including cancer, hepatitis, aberrant mutations, and reproductive issues. Among the 21 identified AFTs, aflatoxin B1 (AFB1) is the most harmful to humans and animals. The mechanisms of AFB1-induced toxicity are connected to the generation of excess reactive oxygen species (ROS), upregulation of CYP450 activities, oxidative stress, lipid peroxidation, apoptosis, mitochondrial dysfunction, autophagy, necrosis, and inflammatory response. Several signaling pathways, including p53, PI3K/Akt/mTOR, Nrf2/ARE, NF-κB, NLRP3, MAPKs, and Wnt/β-catenin have been shown to contribute to AFB1-mediated toxic effects in mammalian cells. Curcumin, a natural product with multiple therapeutic activities (e.g., anti-inflammatory, antioxidant, anticancer, and immunoregulation activities), could revise AFB1-induced harmful effects by targeting these pathways. Therefore, the potential therapeutic use of curcumin against AFB1-related side effects and the underlying molecular mechanisms are summarized. This review, in our opinion, advances significant knowledge, sparks larger discussions, and drives additional improvements in the hazardous examination of AFTs and detoxifying the application of curcumin. Full article
(This article belongs to the Special Issue Dietary Antioxidants and Inflammation-Induced Chronic Diseases)
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