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Molecular Mechanisms and Pharmacological Approaches for Brain Injury
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Molecular Mechanisms and Pharmacological Approaches for Brain Injury

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (20 April 2025) | Viewed by 3504

Special Issue Editor

Dr. Giovanna Casili

E-Mail Website
Guest Editor
Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, 98166 Messina, Italy
Interests: physiological and pharmacological knowledge of inflammatory bowel diseases; spinal cord injuries; brain injuries; neurodegenerative diseases (Alzheimer's and Parkinson's diseases); pain; brain cancer; excellent knowledge of the identification of potential new pharmacological targets in inflammatory, neuro-inflammatory, and neuro-oncological diseases

Special Issue Information

Dear Colleagues,

Brain injury—whether that be stroke, spinal cord injury, traumatic brain injury, seizure, or brain tumors—represents a major cause of death and disability globally. To date, numerous efforts have been made to develop new therapeutics that modulate the pathogenesis of brain injury. Unfortunately, these studies have not led to the successful development and discovery of new drug targets. Therefore, uncovering the molecular mechanisms of injury, recovery, and neuroprotection is important for the development of novel effective therapies. The aim of this Special Issue is to collect up-to-date overviews of the current understandings of brain injury, molecular mechanisms, and pharmacological approaches, as well as the possible clinical translations and therapeutic strategies to treat brain injury. We invite authors to submit original research articles, reviews, and case reports focusing on molecular mechanisms and pharmacological therapies.

Dr. Giovanna Casili
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • molecular mechanisms
  • therapeutical effects
  • brain injury
  • stroke
  • inflammation
  • autophagy
  • drug discover
  • target validation

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Published Papers (2 papers)

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Research

31 pages, 3851 KiB  
Article
Bioactivity and Neuroprotective Effects of Extra Virgin Olive Oil in a Mouse Model of Cerebral Ischemia: An In Vitro and In Vivo Study
by Salvatore Scacco, Silvia Acquaviva, Fábio França Vieira e Silva, John H. Zhang, Lorenzo Lo Muzio, Gaetano Corso, Vito Carlo Alberto Caponio, Pierluigi Reveglia, Lucia Lecce, Maria Eleonora Bizzoca, Prativa Sherchan, Stefania Cantore and Andrea Ballini
Int. J. Mol. Sci. 2025, 26(4), 1771; https://doi.org/10.3390/ijms26041771 - 19 Feb 2025
Viewed by 925
Abstract
Cerebral ischemia is a pathological condition characterized by complete blood and oxygen supply deprivation to neuronal tissue. The ischemic brain compensates for the rapid decline in ATP levels by increasing the anaerobic glycolysis rate, which leads to lactate accumulation and subsequent acidosis. Astrocytes [...] Read more.
Cerebral ischemia is a pathological condition characterized by complete blood and oxygen supply deprivation to neuronal tissue. The ischemic brain compensates for the rapid decline in ATP levels by increasing the anaerobic glycolysis rate, which leads to lactate accumulation and subsequent acidosis. Astrocytes play a critical role in regulating cerebral energy metabolism. Mitochondria are significant targets in hypoxia-ischemia injury, and disruptions in mitochondrial homeostasis and cellular energetics worsen outcomes, especially in the elderly. Elevated levels of n-3 polyunsaturated fatty acids (PUFAs) protect the adult and neonatal brain from ischemic damage by suppressing inflammation, countering oxidative stress, supporting neurovascular unit reconstruction, and promoting oligodendrogenesis. This study examines extra virgin olive oil (EVOO) treatment on TNC WT and TNC M23 cells, focusing on oxygen consumption and reactive oxygen species (ROS) production. This study investigates the effects of different durations of middle cerebral artery occlusion (MCAo) and EVOO administration on cerebral infarct volume, neurological scores, mitochondrial function, and cell viability. Cerebral infarct volume increased with longer ischemia times, while EVOO treatment (0.5 mg/kg/day) significantly reduced infarction across all MCAo durations. The oxygen consumption assays demonstrate EVOO’s dose-dependent stimulation of mitochondrial respiration in astrocytes, particularly at lower concentrations. Furthermore, EVOO-treated cells reduce ROS production during hypoxia, improve cell viability under ischemic stress, and enhance ATP production in ischemic conditions, underscoring EVOO’s neuroprotective potential. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Approaches for Brain Injury)
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14 pages, 3819 KiB  
Article
Regulation of NAD+/NADH Redox Involves the Protective Effects of Ginsenoside Rb1 against Oxygen–Glucose Deprivation/Reoxygenation-Induced Astrocyte Lesions
by Ying Liu, Xi Wang, Jiayu Xie and Minke Tang
Int. J. Mol. Sci. 2023, 24(22), 16059; https://doi.org/10.3390/ijms242216059 - 7 Nov 2023
Cited by 6 | Viewed by 2037
Abstract
The aim of this study was to investigate NAD+/NADH redox regulation in astrocytes by Ginsenoside Rb1 subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) and to reveal the neuroprotective mechanism of ginseng. Neonatal mouse brain was used to culture primary astrocytes. The third generation [...] Read more.
The aim of this study was to investigate NAD+/NADH redox regulation in astrocytes by Ginsenoside Rb1 subjected to oxygen–glucose deprivation/reoxygenation (OGD/R) and to reveal the neuroprotective mechanism of ginseng. Neonatal mouse brain was used to culture primary astrocytes. The third generation of the primary astrocytes was used for the experiments. OGD/R was introduced by culturing the cells in a glucose-free media under nitrogen for 6 h followed by a regular culture for 24 h. Ginsenoside Rb1 attenuated OGD/R-induced astrocyte injury in a dose-dependent manner. It improved the mitochondrial function of OGD/R astrocytes indicated by improving mitochondrial distribution, increasing mitochondrial membrane potential, and enhancing mitochondrial DNA copies and ATP production. Ginsenoside Rb1 significantly lifted intracellular NAD+/NADH, NADPH/NADP+, and GSH/GSSG in OGD/R astrocytes. It inhibited the protein expression of both PARP1 and CD38, while attenuating the SIRT1 drop in OGD/R cells. In line with its effects on PARP1, Ginsenoside Rb1 significantly reduced the expression of poly-ADP-ribosylation (PARylation) proteins in OGD/R cells. Ginsenoside Rb1 also significantly increased the expression of NAMPT and NMNAT2, both of which are key players in NAD/NADH synthesis. The results suggest that the regulation of NAD+/NADH redox involves the protective effects of ginsenoside Rb1 against OGD/R-induced astrocyte injury. Full article
(This article belongs to the Special Issue Molecular Mechanisms and Pharmacological Approaches for Brain Injury)
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