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Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches (4th...
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Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches (4th Edition)

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Immunology and Immunotherapy".

Deadline for manuscript submissions: 31 October 2025 | Viewed by 1824

Special Issue Editor

Dr. Juan Gambini

E-Mail Website
Guest Editor
Freshage Research Group, Department of Physiology, Faculty of Medicine, University of Valencia, E46010 Valencia, Spain
Interests: nutrition; longevity; aging; oxidative stress and exercise
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress and inflammation are two phenomena that are directly involved in practically all pathologies and especially in aging. However, they are not only involved in processes associated with damage. For instance, oxidative stress, which is associated with the redox state, constitutes an important mechanism in cell signaling and many physiological processes. Regarding inflammatory mediators, it is also known that they are essential in mechanisms such as the generation of gastric mucus for the protection of the stomach and the repair of tissues via the mobilization of stem cells. However, when these two phenomena are deregulated, their action is harmful. In this Special Issue, we ask ourselves several questions: How and when should we allow or block oxidative stress and inflammation? What is the advisable anti-inflammatory therapy associated with aging?

Dr. Juan Gambini
Guest Editor

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. Biomedicines 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 2600 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
  • inflammation
  • molecular mechanisms
  • pharmacotherapy
  • longevity
  • aging

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Published Papers (2 papers)

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Research

19 pages, 3157 KiB  
Article
Protective Effects of Nerolidol on Thrombotic Events, Systemic Inflammation, Oxidative Stress, and DNA Damage Following Pulmonary Exposure to Diesel Exhaust Particles
by Naserddine Hamadi, Sumaya Beegam, Nur Elena Zaaba, Ozaz Elzaki, Alreem Alderei, Maha Alfalahi, Shamma Alhefeiti, Dana Alnaqbi, Salama Alshamsi and Abderrahim Nemmar
Biomedicines 2025, 13(3), 729; https://doi.org/10.3390/biomedicines13030729 - 17 Mar 2025
Cited by 1 | Viewed by 413
Abstract
Background/Objectives: Inhalation of environmental particulate air pollution has been reported to cause pulmonary and systemic events including coagulation disturbances, systemic inflammation, and oxidative stress. Nerolidol, a naturally occurring sesquiterpene alcohol, has effective antioxidant and anti-inflammatory effects. Hence, the aim in the present [...] Read more.
Background/Objectives: Inhalation of environmental particulate air pollution has been reported to cause pulmonary and systemic events including coagulation disturbances, systemic inflammation, and oxidative stress. Nerolidol, a naturally occurring sesquiterpene alcohol, has effective antioxidant and anti-inflammatory effects. Hence, the aim in the present investigation was to evaluate the potential ameliorative effects of nerolidol on the coagulation and systemic actions induced by pulmonary exposure to diesel exhaust particles (DEPs). Methods: Nerolidol (100 mg/kg) was given to mice by oral gavage one hour before the intratracheal instillation of DEPs (0.5 mg/kg), and 24 h later various markers of coagulation and systemic toxicity were evaluated. Results: Nerolidol treatment significantly abrogated DEP-induced platelet aggregation in vivo and in vitro. Nerolidol has also prevented the shortening of the prothrombin time and activated plasma thromboplastin time triggered by DEP exposure. Likewise, while the concentrations of fibrinogen and plasminogen activator inhibitor-1 were increased by DEP administration, that of tissue plasminogen activator was significantly decreased. These effects were abolished in the group of mice concomitantly treated with nerolidol and DEP. Moreover, plasma markers of inflammation, oxidative stress, and endothelial dysfunction which were significantly increased in the DEP-treated group, returned to control levels in the nerolidol + DEP group. Nerolidol treatment significantly ameliorated the increase in the concentrations of hypoxia-inducible factor 1α, galectin-3, and neutrophil gelatinase-associated lipocalin induced by pulmonary exposure to DEP. The co-administration of nerolidol + DEPs significantly mitigated the increase in markers of oxidative DNA damage, 8-hydroxy-2-deoxyguanosine, and apoptosis, cleaved-caspase-3, induced by DEP. Conclusions: Collectively, our data demonstrate that nerolidol exert significant ameliorative actions against DEP-induced thrombotic events, endothelial dysfunction, systemic inflammation, oxidative stress, DNA damage, and apoptosis. Pending further pharmacological and toxicological studies, nerolidol could be a promising agent to alleviate the toxicity of inhaled DEPs and other pollutant particles. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches (4th Edition))
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16 pages, 5225 KiB  
Article
Baicalin Decreases the LPS-Induced Intestine Inflammatory Responses by ROS/p-ERK/p-P38 Signal Pathways In Vivo and In Vitro
by Xinyi Sun, Mengru Guo, He Su, Mei Liang, Huining Wu, Linlu Zhao, Jin Zhang, Jieyi He, Yanhong Yong, Zhichao Yu, Xingbin Ma, Xianghong Ju and Xiaoxi Liu
Biomedicines 2025, 13(2), 251; https://doi.org/10.3390/biomedicines13020251 - 21 Jan 2025
Cited by 1 | Viewed by 894
Abstract
Background: This study aimed to investigate the role of ROS/MAPK signaling pathways and the effects of baicalin in LPS-induced inflammatory responses in mice and porcine intestinal epithelial cells (IPEC-J2). Methods: In vivo, 18 male C57BL/6J mice were randomly divided into three groups [...] Read more.
Background: This study aimed to investigate the role of ROS/MAPK signaling pathways and the effects of baicalin in LPS-induced inflammatory responses in mice and porcine intestinal epithelial cells (IPEC-J2). Methods: In vivo, 18 male C57BL/6J mice were randomly divided into three groups (n = 6): control, LPS (3.5 mg/kg LPS administered intraperitoneally [ip] on day 7), and baicalin (200 mg/kg orally for 7 days, with LPS ip on day 7). On day 8, mice were sacrificed, and jejunal tissues were collected for H&E staining. ROS levels in serum and cytokine protein expressions (TNF-α and IL-6) in the jejunum were measured via ELISA, while intestinal MAPK proteins were analyzed using Western blotting. In vitro, the study involved two experimental setups: NAC (a ROS scavenger) and baicalin. For the NAC experiment, IPEC-J2 cells were divided into three groups: control, LPS, and NAC. In the LPS group, cells were treated with LPS (40 μg/mL) for 1 h. In the NAC group, cells were pretreated with NAC prior to LPS exposure. For the baicalin experiment, IPEC-J2 cells were divided into five groups: control, LPS, and baicalin at low (10 μM), medium (20 μM), and high (40 μM) doses. Cells were pretreated with baicalin for 24 h before LPS exposure. ROS/LDH levels and cytokine expressions in the supernatant were determined via ELISA, and MAPK protein expressions were assessed using Western blotting. Results: In vivo, LPS-induced oxidative stress and inflammatory responses in the intestine, reduced the villus height-to-crypt ratio, and significantly increased protein expressions of p-ERK, p-P38, JNK, and p-JNK (p < 0.05). Baicalin treatment significantly inhibited serum ROS levels (p < 0.01), reduced jejunal cytokine expressions (TNF-α and IL-6, p < 0.05), improved intestinal structural damage, and decreased p-ERK, p-P38, and p-JNK protein expressions (p < 0.05). In vitro, NAC significantly reduced ROS levels (p < 0.01), cytokine expressions (TNF-α and IL-6), and MAPK activation (ERK, JNK, P38, and their phosphorylated forms, p < 0.05). Baicalin also significantly decreased ROS (p < 0.05), TNF-α (p < 0.05), IL-6 (p < 0.05), and MAPK protein expressions (ERK, p-ERK, and p-P38, p < 0.05). Molecular docking demonstrated that baicalin effectively bound to ERK and P38 proteins. Conclusions: Baicalin mitigated LPS-induced inflammatory responses via the ROS/p-ERK/p-P38 signaling pathway in vivo and in vitro. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches (4th Edition))
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