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Antioxidants
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Modulation Mechanisms of the Signalling Pathways in the Redox System...
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Modulation Mechanisms of the Signalling Pathways in the Redox System by Natural Products

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 October 2021) | Viewed by 5168

Special Issue Editor

Prof. Dr. Junsei Taira

E-Mail Website
Guest Editor
Department of Bioresources Engineering, National Institute of Technology, Okinawa College, Okinawa 905-2192, Japan
Interests: oxidative stress and modulators; physiologically active substances; antioxidants; anticancer drugs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In a previous Special Issue entitled "Oxidative Stress Modulators and Functional Foods," we published articles for natural products extending beyond the traditional antioxidant role, which are gaining a great deal of attention in functional foods. This research topic in this new Special Issue will be the molecular mechanisms of the modulators’ mediated cell signalling pathways and their potential modulations in relation to various diseases by oxidative stress. Cell signaling transductions are the basic mechanisms of many vital physical processes. Recent studies have revealed that cell signalling transduction, such as nuclear factor erythroid 2-related factor 2/Are (Nrf2/Are), mitogen-activated protein kinases (MAPKs), the nuclear factor kappa B (NF-κB), and protein kinase C (PKC) in the redox system are related to the various physiological actions, such as apoptosis, inflammation, diabetes, cancer and aging. The molecular mechanisms of these actions and the modulation of the signalling pathways in the redox system by natural products and/or synthetic substances will be the focus. This Special Issue will publish reviews and original research papers of both in vitro and in animal models or in humans.

Prof. Dr. Junsei Taira
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

  • oxidative stress
  • antioxidants
  • natural products
  • redox signaling
  • signal transduction
  • reactive oxygen species
  • reactive nitrogen species

Published Papers (2 papers)

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Research

16 pages, 1970 KiB  
Article
Ibogaine-Mediated ROS/Antioxidant Elevation in Isolated Rat Uterus Is β-Adrenergic Receptors and KATP Channels Mediated
by Nikola Tatalović, Teodora Vidonja Uzelac, Zorana Oreščanin Dušić, Aleksandra Nikolić-Kokić, Mara Bresjanac and Duško Blagojević
Antioxidants 2021, 10(11), 1792; https://doi.org/10.3390/antiox10111792 - 09 Nov 2021
Cited by 3 | Viewed by 1830
Abstract
Ibogaine effects are mediated by cellular receptors, ATP depletion followed by ROS production and antioxidant enzyme activity elevation in a dose and time dependent manner. Since the role of KATP channels and β-adrenoceptors in ROS cellular circuit was established here we explored [...] Read more.
Ibogaine effects are mediated by cellular receptors, ATP depletion followed by ROS production and antioxidant enzyme activity elevation in a dose and time dependent manner. Since the role of KATP channels and β-adrenoceptors in ROS cellular circuit was established here we explored their role in ibogaine pro-antioxidant effectiveness. Single dose of ibogaine (10 mg/L i.e., 28.8 μmol/L) was applied to isolated rat uterus (spontaneous and Ca2+-stimulated) and contractility and antioxidant enzymes activity were monitored during 4 h. Ibogaine increased amplitude and frequency of spontaneous active uteri immediately after addition that was prevented by propranolol (β1 and β2 adrenoceptors selective antagonists) and glibenclamide (KATP sensitive channels inhibitor; only frequency) pre-treatment. In Ca2+-stimulated uteri, ibogaine decreased both amplitude and frequency after 4 h. Pre-treatment with propranolol abolished ibogaine induced amplitude lowering, while glibenclamide had no effect. In both types of active uterus, ibogaine induced a decrease in SOD1 and an increase in CAT activity after 2 h. In Ca2+-stimulated uterus, there was also a decrease of SOD2 activity after 2 h. After 4 h, SOD1 activity returned to the baseline level, but GSH-Px activity increased. Pre-treatment with both propranolol and glibenclamide abolished observed changes of antioxidant enzymes activity suggesting that ibogaine pro-antioxidative effectiveness is β-adrenergic receptors and KATP channels mediated. Full article
(This article belongs to the Special Issue Modulation Mechanisms of the Signalling Pathways in the Redox System by Natural Products)
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16 pages, 5168 KiB  
Article
Anti-NAFLD Effect of Djulis Hull and Its Major Compound, Rutin, in Mice with High-Fat Diet (HFD)-Induced Obesity
by Yu-Tang Tung, Jun-Lan Zeng, Shang-Tse Ho, Jin-Wei Xu, Shiming Li and Jyh-Horng Wu
Antioxidants 2021, 10(11), 1694; https://doi.org/10.3390/antiox10111694 - 27 Oct 2021
Cited by 14 | Viewed by 2813
Abstract
Nonalcoholic fatty liver disease (NAFLD) has become the main cause of chronic liver disease worldwide, and the increasing trend of NAFLD has burdened the healthcare system. NAFLD encompasses a wide range of liver pathologies, from simple benign hepatocyte steatosis to more severe inflammatory [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) has become the main cause of chronic liver disease worldwide, and the increasing trend of NAFLD has burdened the healthcare system. NAFLD encompasses a wide range of liver pathologies, from simple benign hepatocyte steatosis to more severe inflammatory nonalcoholic steatohepatitis. Djulis (Chenopodium formosanum Koidz.) is traditionally used as a native cereal and a food supplement that promotes human health through its antioxidant, hepatoprotection, skin protection, hypolipidemic, hypoglycemic, and antitumor effects. Djulis hull, regarded as agricultural waste, is usually removed during food processing and contains high rutin content. The present study evaluated the anti-NAFLD effect of Djulis hull and its major compound, rutin, in mice with high-fat diet (HFD)-induced obesity. Male C57BL/6J mice were randomly divided into one of five diet groups (n = 6 per group) and fed the following for 16 weeks: (1) normal diet group (ND), (2) HFD group (HFD), (3) HFD and oral gavage of low dose (50 mg/kg) of Djulis hull crude extract group (HFD/LCE), (4) HFD and oral gavage of high dose (250 mg/kg) of Djulis hull crude extract group (HFD/HCE), or (5) HFD and oral gavage (50 mg/kg) of rutin (HFD/R) group. We found that Djulis hull crude extract markedly reduced HFD-induced elevation in body weight and fat around the kidney weights, hepatic injury indicators (AST and ALT), and steatosis and hypertrophy. Furthermore, Djulis hull crude extract administration significantly affected DG(20:4/18:1), PA(22:0/17:1), PC(10:0/17:0), and PA(18:4/20:5) in HFD-induced obese mice. In addition, treating HFD-induced obese rats with Djulis hull crude extract significantly increased fatty acid oxidation by increasing the protein expression of phosphorylated AMP-activated protein kinase, peroxisome proliferator-activated receptor-α, and hepatic carnitine palmitoyltransferase-1 in the liver. Moreover, the administration of Djulis hull crude extract significantly decreased the inflammatory response (PPARγ, IL-6, and TNF-α) to modulate oxidative damage. Therefore, Djulis hull crude extract attenuated the progression of NAFLD by reducing inflammation mediated by PPARγ and enhancing the expression levels of genes involved in fatty acid oxidation mediated by AMPK signaling. Full article
(This article belongs to the Special Issue Modulation Mechanisms of the Signalling Pathways in the Redox System by Natural Products)
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