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Antioxidants
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Free Radicals, Antioxidants, and Oxidative Stress in Aging and Age-Related...
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Free Radicals, Antioxidants, and Oxidative Stress in Aging and Age-Related Diseases—2nd Edition

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: 31 May 2025 | Viewed by 1876

Special Issue Editors

Prof. Dr. Abdelouahed Khalil

E-Mail Website
Guest Editor
Research Centre on Aging, Department of Medicine, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, QC, Canada
Interests: aging; atherosclerosis; lipoproteins; inflammation; antioxidants
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Tamas Fulop

E-Mail Website
Guest Editor
Research Centre on Aging, Department of Medicine, Faculty of Medicine and Health Sciences, University of Sherbrooke, Sherbrooke, QC, Canada
Interests: aging; inflammaging; immune response; Alzheimer’s disease; free radicals; cancer

Special Issue Information

Dear Colleagues,

Our previous edition received an overwhelming number of submissions and was a successful compilation of research and review articles. Therefore, I am pleased to announce the second edition of our Special Issue entitled “Free Radicals, Antioxidants, and Oxidative Stress in Aging and Age-Related Diseases”.

The second edition of this Special Issue delves into the intricate balance between oxidative stress and antioxidant defenses in the aging process and associated diseases. This edition compiles the latest research exploring how free radicals, highly reactive molecules produced during metabolism, contribute to cellular damage and the progression of age-related diseases such as Alzheimer's disease, cardiovascular disorders, and cancer. The purpose of this Special Issue continues to review the current state of our knowledge regarding the effect of free radicals on the aging process and age-related diseases. Particular attention will also be given to studies on the effect of antioxidants in reducing the damage induced by ROS and in preventing the development of certain physio-pathological alterations.

Prof. Dr. Abdelouahed Khalil
Prof. Dr. Tamas Fulop
Guest Editors

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

  • aging
  • oxidative stress
  • age-related diseases

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Published Papers (2 papers)

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Research

15 pages, 3663 KiB  
Article
Roasted Astragalus membranaceus Inhibits Aβ25–35-Induced Oxidative Stress in Neuronal Cells by Activating the Nrf2/HO-1 and AKT/CREB/BDNF Pathways
by Yun-Jeong Ji, Min Hye Kang, Sin Hee Han, Geum-Soog Kim, Hyung Don Kim and Gwi Yeong Jang
Antioxidants 2024, 13(11), 1311; https://doi.org/10.3390/antiox13111311 - 28 Oct 2024
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Abstract
(1) Background: Astragalus membranaceus (AM) has antioxidant and anti-inflammatory effects, but its specific mechanism of action in the brain is still unclear. In this study, we developed a roasting process to maximize the cognitive improvement impact of AM. We focused on enhancing physiological [...] Read more.
(1) Background: Astragalus membranaceus (AM) has antioxidant and anti-inflammatory effects, but its specific mechanism of action in the brain is still unclear. In this study, we developed a roasting process to maximize the cognitive improvement impact of AM. We focused on enhancing physiological activity to enhance the brain neuron protection effect and alleviate neuronal damage caused by neurodegenerative diseases. (2) Methods: AM was roasted at 260 °C for 20, 30, or 40 min, and the hot water extracts were tested on HT22 cells for ROS levels, apoptosis, and antioxidant protein expression. The effect on the BDNF-AKT-CREB pathway under stress was also analyzed. (3) Results: Roasted AM decreased ROS production and the expression of apoptosis-related factors while activating the expression of antioxidant proteins in HT22 cells treated with Aβ25–35. In particular, 30 min roasting (R-AM2) significantly reduced ROS production, inhibited cell death, and increased antioxidant protein expression. The Nrf2 pathway was activated Bax, and cleaved caspase-3 levels were reduced. BDNF and p-CREB expression were increased by 20% and 50–70%, respectively. In the MAPK pathway, p-ERK levels were increased by 30%, and p-P38 levels were increased by approximately 20%. (4) Conclusions: These findings suggest that roasted AM upregulates brain-derived neurotrophic factor (BDNF) in HT22 cells, providing neuroprotective effects by activating the AKT/CREB/BDNF pathway and inhibiting neuronal apoptosis. Therefore, roasted AM shows potential as a neuroprotective agent for preventing or treating neurodegenerative diseases, such as Alzheimer’s, linked to BDNF deficiency. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants, and Oxidative Stress in Aging and Age-Related Diseases—2nd Edition)
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23 pages, 17221 KiB  
Article
Aged Gut Microbiome Induces Metabolic Impairment and Hallmarks of Vascular and Intestinal Aging in Young Mice
by Chak-Kwong Cheng, Lianwei Ye, Yuanyuan Zuo, Yaling Wang, Li Wang, Fuyong Li, Sheng Chen and Yu Huang
Antioxidants 2024, 13(10), 1250; https://doi.org/10.3390/antiox13101250 - 17 Oct 2024
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Abstract
Aging, an independent risk factor for cardiometabolic diseases, refers to a progressive deterioration in physiological function, characterized by 12 established hallmarks. Vascular aging is driven by endothelial dysfunction, telomere dysfunction, oxidative stress, and vascular inflammation. This study investigated whether aged gut microbiome promotes [...] Read more.
Aging, an independent risk factor for cardiometabolic diseases, refers to a progressive deterioration in physiological function, characterized by 12 established hallmarks. Vascular aging is driven by endothelial dysfunction, telomere dysfunction, oxidative stress, and vascular inflammation. This study investigated whether aged gut microbiome promotes vascular aging and metabolic impairment. Fecal microbiome transfer (FMT) was conducted from aged (>75 weeks old) to young C57BL/6 mice (8 weeks old) for 6 weeks. Wire myography was used to evaluate endothelial function in aortas and mesenteric arteries. ROS levels were measured by dihydroethidium (DHE) staining and lucigenin-enhanced chemiluminescence. Vascular and intestinal telomere function, in terms of relative telomere length, telomerase reverse transcriptase expression and telomerase activity, were measured. Systemic inflammation, endotoxemia and intestinal integrity of mice were assessed. Gut microbiome profiles were studied by 16S rRNA sequencing. Some middle-aged mice (40–42 weeks old) were subjected to chronic metformin treatment and exercise training for 4 weeks to evaluate their anti-aging benefits. Six-week FMT impaired glucose homeostasis and caused vascular dysfunction in aortas and mesenteric arteries in young mice. FMT triggered vascular inflammation and oxidative stress, along with declined telomerase activity and shorter telomere length in aortas. Additionally, FMT impaired intestinal integrity, and triggered AMPK inactivation and telomere dysfunction in intestines, potentially attributed to the altered gut microbial profiles. Metformin treatment and moderate exercise improved integrity, AMPK activation and telomere function in mouse intestines. Our data highlight aged microbiome as a mechanism that accelerates intestinal and vascular aging, suggesting the gut-vascular connection as a potential intervention target against cardiovascular aging and complications. Full article
(This article belongs to the Special Issue Free Radicals, Antioxidants, and Oxidative Stress in Aging and Age-Related Diseases—2nd Edition)
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