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Brain Sciences
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The Role of Glia in Inflammatory Processes
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The Role of Glia in Inflammatory Processes

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuroglia".

Deadline for manuscript submissions: 16 February 2026 | Viewed by 2737

Special Issue Editors

Dr. Charles Elias Assmann

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, Federal University of Santa Maria, Santa Maria, Brazil
Interests: neuroinflammation; neurodegenerative diseases; psychiatric disorders; purinergic signaling; bioactive compounds; toxicology
Dr. Margarete Dulce Bagatini

E-Mail Website
Guest Editor
Graduate Program in Medical Sciences, Federal University of Fronteira Sul, Chapecó 89815-899, SC, Brazil
Interests: oxidative stress; purinergic system; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Central nervous system (CNS) inflammation is a crucial process for brain homeostasis. Microglial cells and astrocytes are among the main players with pivotal functions in controlling inflammatory responses and promoting tissue repair. Although inflammation can be beneficial for the brain, exacerbated responses have been associated with the development of neurological conditions. Despite advances in the understanding of neuroinflammatory processes and the role of glial cells in the brain, much is still lacking in the comprehension of the specific pathways involved in this mechanism. Moreover, the development of better diagnostic tools and therapies is of significance to improve the quality of life of patients with neurological conditions.

The main purpose of this Special Issue of Brain Sciences is to provide high-quality research on the rapidly growing field of the function of glial cells in inflammatory processes.

Recent progress in the comprehension of the underlying mechanisms involved in CNS inflammation and the role of microglia and astrocytes will be of particular importance.

We also welcome contributions exploring specific signaling pathways involved in inflammatory responses such as oxidative and nitrosative stress and purinergic signaling. Pharmacological and non-pharmacological strategies, including those focusing on bioactive and natural compounds, and diagnostic tools are also of interest.

The scope of this Special Issue welcomes submissions of original research works, brief reports, case studies, clinical trials, perspectives, mini-reviews, reviews, short communications, and translational research articles. Data may be obtained from human subjects and in vitro and in vivo protocols using different organism models.

Potential topics include, but are not limited to, the following:

  • The role of glial cells in CNS inflammation;
  • The signaling pathways involved in neuroinflammation;
  • Neuroinflammation in neurodegenerative and psychiatric disorders;
  • Behavioral alterations;
  • Oxidative and nitrosative stress;
  • Pharmacological and non-pharmacological interventions;
  • Cutting-edge neuroimaging techniques.

We aim to provide state-of-the-art research exploring the role of microglia and astrocytes in the underlying mechanisms involved in CNS inflammation.

Dr. Charles Elias Assmann
Dr. Margarete Dulce Bagatini
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. Brain Sciences 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 2200 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

  • neuroinflammation
  • neurodegenerative and psychiatric disorders
  • microglia
  • astrocytes
  • purinergic signaling
  • bioactive and natural compounds
  • immunopharmacology and immunotoxicology
  • oxidative and nitrosative stress
  • neuroimaging
  • neuroscience and behavior

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Published Papers (3 papers)

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Research

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15 pages, 3366 KiB  
Article
ATP Alters the Oxylipin Profiles in Astrocytes: Modulation by High Glucose and Metformin
by Alexey I. Drozhdev, Vladislav O. Gorbatenko, Sergey V. Goriainov, Dmitry V. Chistyakov and Marina G. Sergeeva
Brain Sci. 2025, 15(3), 293; https://doi.org/10.3390/brainsci15030293 - 11 Mar 2025
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Abstract
Background: Astrocytes play a key role in the inflammatory process accompanying various neurological diseases. Extracellular ATP accompanies inflammatory processes in the brain, but its effect on lipid mediators (oxylipins) in astrocytes remains elusive. Metformin is a hypoglycemic drug with an anti-inflammatory effect that [...] Read more.
Background: Astrocytes play a key role in the inflammatory process accompanying various neurological diseases. Extracellular ATP accompanies inflammatory processes in the brain, but its effect on lipid mediators (oxylipins) in astrocytes remains elusive. Metformin is a hypoglycemic drug with an anti-inflammatory effect that has been actively investigated in the context of therapy for neuroinflammation, but its mechanisms of action are not fully elucidated. Therefore, we aimed to characterize the effects of ATP on inflammatory markers and oxylipin profiles; determine the dependence of these effects on the adaptation of astrocytes to high glucose levels; and evaluate the possibility of modulating ATP effects using metformin. Methods: We estimated the ATP-mediated response of primary rat astrocytes cultured at normal (NG, 5 mM) and high (HG, 22.5 mM) glucose concentrations for 48 h before stimulation. Cell responses were assessed by monitoring changes in the expression of inflammatory markers (TNFα, IL-6, IL-10, IL-1β, iNOS, and COX-2) and the synthesis of oxylipins (41 compounds), assayed with ultra-high-performance liquid chromatography and tandem mass spectrometry (UPLC-MS/MS). Intracellular pathways were assessed by analyzing the phosphorylation of p38; ERK MAPK; transcription factors STAT3 and NF-κB; and the enzymes mediating oxylipin synthesis, COX-1 and cPLA2. Results: The stimulation of cells with ATP does not affect the expression of pro-inflammatory markers, increases the activities of p38 and ERK MAPKs, and activates oxylipin synthesis, shifting the profiles toward an increase in anti-inflammatory compounds (PGD2, PGA2, 12-HHT, and 18-HEPE). The ATP effects are reduced in HG astrocytes. Metformin potentiated ATP-induced oxylipin synthesis (11-HETE, PGD2, 12-HHT, 15-HETE, 13-HDoHE, and 15-HETrE), which was predominantly evident in NG cells. Conclusions: Our data provide new evidence showing that ATP induces the release of anti-inflammatory oxylipins, and metformin enhances these effects. These results should be considered in the development of anti-inflammatory therapeutic approaches aimed at modulating astrocyte function in various pathologies. Full article
(This article belongs to the Special Issue The Role of Glia in Inflammatory Processes)
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17 pages, 3639 KiB  
Article
Lycorine Pre-Treatment Alleviates Microglia Inflammation After Cerebral Ischemia by Inhibiting NF-κB Phosphorylation
by Wuyan Zheng, Wanyu Wu, Yuhan Li, Bo Qin, Yuping Wang, Yunhan Zeng, Betty Yuen Kwan Law and Vincent Kam Wai Wong
Brain Sci. 2025, 15(3), 290; https://doi.org/10.3390/brainsci15030290 - 9 Mar 2025
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Abstract
Background: Middle-aged and elderly individuals may experience detrimental health effects due to ischemic stroke (IS). The inflammatory response triggered during IS exacerbates neuronal damage, becoming a barrier to effective IS treatment and leading to poor patient prognosis. Nevertheless, the specific role of microglia [...] Read more.
Background: Middle-aged and elderly individuals may experience detrimental health effects due to ischemic stroke (IS). The inflammatory response triggered during IS exacerbates neuronal damage, becoming a barrier to effective IS treatment and leading to poor patient prognosis. Nevertheless, the specific role of microglia in the inflammatory response triggered by IS remains mostly unclear. The primary target of this investigation is to study the neuroinflammatory impact of lycorine (LYC) during the IS process. Our objective is to evaluate whether LYC deploys its anti-inflammatory effect with modulation of the NF-κB signaling pathway, thereby reducing IS symptoms. Methods: In this research, BV-2 cells were pre-treated with LYC for 24 h before LPS was added to induce inflammation. Results: It has been discovered that LYC suppresses BV-2 cell polarization and reduces the levels of inflammatory cytokines (IL-1β, IL-6, TNF-α), showing its potential anti-inflammatory effects in vitro. Furthermore, IκBα and p65 play crucial roles in regulating the inflammatory response within the NF-κB signaling pathway. Mechanistic exploration indicates that LYC can activate the expression of IκBα in LPS-induced BV-2 cells. IκBα inhibits NF-κB by binding to its p65 subunit, sequestering it in the cytoplasm and preventing its translocation to the nucleus, thereby inhibiting inflammation. Additionally, p65 is a key transcription factor for pro-inflammatory genes, and its downregulation leads to decreased transcriptional activity of these genes. The combined effect of increased IκBα and decreased p65 results in significantly reduced NF-κB activity, thereby alleviating the inflammatory response. Meanwhile, in vivo studies indicate that LYC pre-treatment significantly reduces the infarct size caused by middle cerebral artery occlusion (MCAO) in rats. The assessment of cerebral infarction volume, neurological scores, brain edema rate and inflammation levels in MCAO rats pre-treated with LYC indicates positive therapeutic effects. Conclusions: In summary, our research indicates that LYC pre-treatment has significant anti-inflammatory effects by attenuating inflammation levels through NF-κB inhibition, which contributes to potential therapeutic benefits in ischemic stroke (IS) and may improve disease prognosis. LYC may serve as an adjunctive clinical pre-treatment for IS, which has to be confirmed by clinical trials in the future. Full article
(This article belongs to the Special Issue The Role of Glia in Inflammatory Processes)
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Review

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11 pages, 936 KiB  
Review
The Neuroprotective Role of A2A Adenosine Purinoceptor Modulation as a Strategy Against Glioblastoma
by Júlia Leão Batista Simões, Geórgia de Carvalho Braga, Michelli Fontana, Charles Elias Assmann and Margarete Dulce Bagatini
Brain Sci. 2024, 14(12), 1286; https://doi.org/10.3390/brainsci14121286 - 21 Dec 2024
Viewed by 853
Abstract
Glioblastoma (GBM) is a highly lethal type of cancer, frequently presenting an unfavorable prognosis. The current treatment options for this neoplasia are still limited, highlighting the need for further research evaluating new drugs to treat GBM or to serve as an adjuvant to [...] Read more.
Glioblastoma (GBM) is a highly lethal type of cancer, frequently presenting an unfavorable prognosis. The current treatment options for this neoplasia are still limited, highlighting the need for further research evaluating new drugs to treat GBM or to serve as an adjuvant to improve the efficiency of currently used therapies. In this sense, the inhibition of A2A receptors in the brain has presented a neuroprotective role for several diseases, such as neurodegenerative conditions, and it has been suggested as a possible pharmacological target in some types of cancer; thus, it also can be underscored as a potential target in GBM. Recently, Istradefylline (IST) was approved by the FDA for treating Parkinson’s disease, representing a safe drug that acts through the inhibition of the A2A receptor, and it has also been suggested as an antineoplastic drug. Therefore, this work aims to explore the effects of A2A receptor inhibition as a therapy for GBM and assess the feasibility of this blockage occurring through the effects of IST. Full article
(This article belongs to the Special Issue The Role of Glia in Inflammatory Processes)
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