Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Neurobiology and Clinical Neuroscience".

Deadline for manuscript submissions: 31 July 2024 | Viewed by 965

Special Issue Editor


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Guest Editor
School of Optometry, The Hong Kong Polytechnic University, Kowloon, Hong Kong
Interests: neurodegenerative disorders; regenerative medicine; aging-related disorder; anti-inflammatory therapy; mitochondrial augmentation

Special Issue Information

Dear Colleagues,

This Special Issue provides a comprehensive overview of the current information in the field of neuroinflammation. Neuroinflammation is a complex process that involves the activation of immune cells in the central nervous system which can contribute to the development and progression of a wide range of neurological disorders, including Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and stroke.

This Special Issue will cover a wide range of topics related to neuroinflammation, including, but not limited to, the molecular mechanism of neuroinflammation, the process of neuroinflammation, and the potential therapeutic strategies for treating neuroinflammatory diseases. The Special Issue also includes a discussion on the potential of various therapeutic strategies for treating diseases via targeting neuroinflammation, including, but not limited to, anti-inflammatory drugs, immunomodulatory therapies, and stem cell-based therapies.

Overall, this Special Issue provides a valuable resource for researchers and clinicians interested in neuroinflammation, highlighting the importance of continued research in understanding the underlying pathophysiological mechanisms and developing effective therapeutic strategies for neuroinflammatory diseases.

Dr. Li-Ping Zhou
Guest Editor

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Keywords

  • neuroinflammation
  • molecular mechanism
  • anti-inflammation
  • stem cell-based therapy
  • cell-free stem-cell-based therapy
  • immunomodulation

Published Papers (2 papers)

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Research

30 pages, 20372 KiB  
Article
Possible Prophylactic Effects of Sulforaphane on LPS-Induced Recognition Memory Impairment Mediated by Regulating Oxidative Stress and Neuroinflammatory Proteins in the Prefrontal Cortex Region of the Brain
by Noor Ahmed Alzahrani, Khulud Abdullah Bahaidrah, Rasha A. Mansouri, Rahaf Saeed Aldhahri, Gamal S. Abd El-Aziz and Badrah S. Alghamdi
Biomedicines 2024, 12(5), 1107; https://doi.org/10.3390/biomedicines12051107 - 16 May 2024
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Abstract
Background: Alzheimer’s disease (AD) presents a significant global health concern, characterized by neurodegeneration and cognitive decline. Neuroinflammation is a crucial factor in AD development and progression, yet effective pharmacotherapy remains elusive. Sulforaphane (SFN), derived from cruciferous vegetables and mainly from broccoli, has shown [...] Read more.
Background: Alzheimer’s disease (AD) presents a significant global health concern, characterized by neurodegeneration and cognitive decline. Neuroinflammation is a crucial factor in AD development and progression, yet effective pharmacotherapy remains elusive. Sulforaphane (SFN), derived from cruciferous vegetables and mainly from broccoli, has shown a promising effect via in vitro and in vivo studies as a potential treatment for AD. This study aims to investigate the possible prophylactic mechanisms of SFN against prefrontal cortex (PFC)-related recognition memory impairment induced by lipopolysaccharide (LPS) administration. Methodology: Thirty-six Swiss (SWR/J) mice weighing 18–25 g were divided into three groups (n = 12 per group): a control group (vehicle), an LPS group (0.75 mg/kg of LPS), and an LPS + SFN group (25 mg/kg of SFN). The total duration of the study was 3 weeks, during which mice underwent treatments for the initial 2 weeks, with daily monitoring of body weight and temperature. Behavioral assessments via novel object recognition (NOR) and temporal order recognition (TOR) tasks were conducted in the final week of the study. Inflammatory markers (IL-6 and TNF), antioxidant enzymes (SOD, GSH, and CAT), and pro-oxidant (MDA) level, in addition to acetylcholine esterase (AChE) activity and active (caspase-3) and phosphorylated (AMPK) levels, were evaluated. Further, PFC neuronal degeneration, Aβ content, and microglial activation were also examined using H&E, Congo red staining, and Iba1 immunohistochemistry, respectively. Results: SFN pretreatment significantly improved recognition memory performance during the NOR and TOR tests. Moreover, SFN was protected from neuroinflammation and oxidative stress as well as neurodegeneration, Aβ accumulation, and microglial hyperactivity. Conclusion: The obtained results suggested that SFN has a potential protective property to mitigate the behavioral and biochemical impairments induced by chronic LPS administration and suggested to be via an AMPK/caspase-3-dependent manner. Full article
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16 pages, 8262 KiB  
Article
Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling
by Federica Mannino, Valentina Urzì Brancati, Rita Lauro, Igor Pirrotta, Michelangelo Rottura, Natasha Irrera, Gian Maria Cavallini, Giovanni Pallio, Eloisa Gitto and Sara Manti
Biomedicines 2024, 12(5), 1009; https://doi.org/10.3390/biomedicines12051009 - 3 May 2024
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Abstract
Hypovolemic shock is a circulatory failure, due to a loss in the effective circulating blood volume, that causes tissue hypoperfusion and hypoxia. This condition stimulates reactive oxygen species (ROS) and pro-inflammatory cytokine production in different organs and also in the central nervous system [...] Read more.
Hypovolemic shock is a circulatory failure, due to a loss in the effective circulating blood volume, that causes tissue hypoperfusion and hypoxia. This condition stimulates reactive oxygen species (ROS) and pro-inflammatory cytokine production in different organs and also in the central nervous system (CNS). Levosimendan, a cardioprotective inodilator, and dobutamine, a β1-adrenergic agonist, are commonly used for the treatment of hypovolemic shock, thanks to their anti-inflammatory and antioxidant effects. For this reason, we aimed at investigating levosimendan and dobutamine’s neuroprotective effects in an “in vitro” model of lipopolysaccharide (LPS)-induced neuroinflammation. Human microglial cells (HMC3) were challenged with LPS (0.1 µg/mL) to induce an inflammatory phenotype and then treated with levosimendan (10 µM) or dobutamine (50 µM) for 24 h. Levosimendan and dobutamine significantly reduced the ROS levels and markedly increased Nrf2 and HO-1 protein expression in LPS-challenged cells. Levosimendan and dobutamine also decreased p-NF-κB expression and turned off the NLRP3 inflammasome together with its downstream signals, caspase-1 and IL-1β. Moreover, a reduction in TNF-α and IL-6 expression and an increase in IL-10 levels in LPS-stimulated HMC3 cells was observed following treatment. In conclusion, levosimendan and dobutamine attenuated LPS-induced neuroinflammation through NF-κB pathway inhibition and NLRP3 inflammasome activation via Nrf2/HO-1 signalling, suggesting that these drugs could represent a promising therapeutic approach for the treatment of neuroinflammation consequent to hypovolemic shock. Full article
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