Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
3.7
4.7
Journals
Biomedicines
Special Issues
Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies
share announcement

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 595

Special Issue Editor

Dr. Li-Ping Zhou

E-Mail Website
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

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. 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

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

Published Papers (1 paper)

Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

16 pages, 6195 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
Viewed by 426
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
(This article belongs to the Special Issue Neuroinflammation: From Pathophysiologic Mechanisms to Therapeutic Strategies)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-1
Back to TopTop