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Natural Antioxidants Are Associated with ROS and Diseases

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

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 5836

Special Issue Editors


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Guest Editor
School of Medicine, Chung Shan Medical University, Taichung City 40201, Taiwan
Interests: natural antioxidants; reactive oxygen species (ROS); mitochondrial biogenesis; antioxidant effects; anti-inflammatory, anti-cancer, anti-apoptotic, and anti-autophagy properties
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Nursing, Division of Basic Medical Sciences, Chang Gung University of Science and Technology, Taoyuan, Taiwan
Interests: the mechanism of mediated signaling cascades that preventive strategy that aims to inhibit, delay, or reverse the disorder of metabolic functions and carcinogenesis; using naturally extracted or synthetic chemical agents; such as various phytochemicals

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Guest Editor
1. Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 40402, Taiwan
2. Department of Optometry, Asia University, Taichung 41354, Taiwan
Interests: age-related macular; degeneration; human retinal pigment epithelium; apoptosis; autophagy; mitochondrial membrane potential

Special Issue Information

Dear Colleagues,

In the cell system, the production of reactive oxygen species (ROS) can cause cell damage, affect the structure and function of membrane lipids, proteins and nucleic acids, and ultimately lead to cell death. Previous studies have shown that inhibiting ROS-induced cell damage may inhibit disease generation. ROS is considered to be an important mechanism leading to a variety of diseases, such as infections, eye diseases such as diabetic retinopathy (DR), and age-related macular degeneration (AMD), as well as brain, lung, colorectal, and liver cancers. Antioxidants and anti-inflammatory agents have been shown to protect health, such as flavonoids and phenolic acids, and their derivatives, carotenoids, terpenoids, vitamins, and others have been identified and quantified in various plants. To further clarify the basic molecular mechanism of antioxidants in the process of disease and to further understand their interaction may pave the way for new treatment strategies for diseases. This Special Issue focuses on how natural antioxidants regulate ROS to downregulate the onset of diseases.

Prof. Dr. Yuan-Yen Chang
Prof. Dr. Hsing-Chun Kuo
Prof. Dr. Hui-Wen Lin
Guest Editors

Manuscript Submission Information

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Keywords

  • natural antioxidants
  • reactive oxygen species (ROS)
  • mitochondrial biogenesis
  • antioxidant effects
  • anti-inflammatory
  • anti-cancer
  • anti-apoptotic
  • anti-autophagy

Published Papers (2 papers)

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Research

13 pages, 2994 KiB  
Article
Glucogallin Attenuates RAW 264.7 Cells from Arsenic Trioxide Induced Toxicity via the NF-ҡB/NLRP3 Pathway
by Anam Najib Khan, Rajveer Singh, Arka Bhattacharya, Sonu Kumar, Arijit Ghosh, Debasish Nag, Velayutham Ravichandiran and Dipanjan Ghosh
Molecules 2022, 27(16), 5263; https://doi.org/10.3390/molecules27165263 - 18 Aug 2022
Cited by 4 | Viewed by 2394
Abstract
Chronic arsenic (As) poisoning is mostly due to subsoil water contaminated with As and its salts. Exposure to As has been found to cause an elevation in reactive oxygen species (ROS), leading to the damage of DNA and proteins, and it also causes [...] Read more.
Chronic arsenic (As) poisoning is mostly due to subsoil water contaminated with As and its salts. Exposure to As has been found to cause an elevation in reactive oxygen species (ROS), leading to the damage of DNA and proteins, and it also causes immunotoxicity. Treatment regimens are primarily based on chelation therapy and amino acid and vitamin supplementations. Recent studies have established that natural products display effective and progressive relief from arsenicosis without any side effects. β-glucogallin (BGG), a gallo-tannin natural product, is reported to possess anti-oxidant and anti-inflammatory properties. In the present study, we aim to observe the protective role of BGG against As-induced cytotoxicity, apoptosis, mitochondrial dysfunction, and the underlying mechanisms in RAW 264.7 macrophage cells. We found that BGG alleviates As-induced ROS, apoptosis, and mitochondrial dysfunction in RAW 264.7 macrophage cells. Thus, BGG can be used therapeutically to prevent As-induced toxicity. Full article
(This article belongs to the Special Issue Natural Antioxidants Are Associated with ROS and Diseases)
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14 pages, 21150 KiB  
Article
AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity
by Chia-Yu Hung, Chih-Han Chang, Tzu-Jung Lin, Hsin-Hui Yi, Nian-Zhen Tsai, Yu-Ru Chen and Yng-Tay Chen
Molecules 2022, 27(3), 1066; https://doi.org/10.3390/molecules27031066 - 4 Feb 2022
Cited by 4 | Viewed by 2168
Abstract
Acrylamide (ACR) is present in high-temperature-processed high-carbohydrate foods, cigarette smoke, and industrial pollution. Chronic exposure to ACR may induce neurotoxicity from reactive oxygen species (ROS); however, the mechanisms underlying ACR-induced neurotoxicity remain unclear. We studied 28-day subacute ACR toxicity by repeatedly feeding ACR [...] Read more.
Acrylamide (ACR) is present in high-temperature-processed high-carbohydrate foods, cigarette smoke, and industrial pollution. Chronic exposure to ACR may induce neurotoxicity from reactive oxygen species (ROS); however, the mechanisms underlying ACR-induced neurotoxicity remain unclear. We studied 28-day subacute ACR toxicity by repeatedly feeding ACR (0, 15, or 30 mg/kg) to rats. We conducted RNA sequencing and Western blot analyses to identify differences in mRNA expression in the blood and in protein expression in the brain tissues, respectively, of the rats. AQP4 transient transfection was performed to identify potential associations with protein regulation. The rats treated with 30 mg/kg ACR exhibited hind-limb muscle weakness. Matrix metalloproteinase (MMP9) expression was higher in the ACR-treated group than in the control group. ACR induced MMP-9 and AQP4 protein expression in the brain tissues of the rats, which subsequently presented with neurotoxicity. In the in vitro study, Neuro-2a cells were transiently transfected with AQP4, which inhibited MMP-9 and TNF receptor-associated factor 6 (TRAF6) expression, and inhibited ACR induced expression of TRAF6, IκBα, and nuclear factor κB (NFκB). Using a combination of in vivo and in vitro experiments, this study revealed that depressive symptoms associated with ACR-induced neurotoxicity are associated with downregulation of AQP4 and induction of the TRAF6 pathway. Full article
(This article belongs to the Special Issue Natural Antioxidants Are Associated with ROS and Diseases)
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