Pharmacological Targets for Neuroinflammation

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 3058

Special Issue Editor


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Guest Editor
NICM Health Research Institute, Western Sydney University, Westmead, NSW 2145, Australia
Interests: inflammation and neuroinflammation; natural products; synergistic interaction; cardiovascular diseases; drug-herb interaction

Special Issue Information

Dear Colleagues,

Neuroinflammation is the process of inflammation that occurs in the brain or central nervous system and is believed to play a critical role in various neurological disorders, such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and stroke. This complex process involves several key players, including microglia, astrocytes, pro-inflammatory cytokines (e.g., interleukin-1β, tumor necrosis factor-alpha), and other immune mediators.

The focus of this Special Issue is to gather new breakthrough research findings on various pharmacological targets that have been identified to modulate neuroinflammation and explore their possible crosstalk. We welcome preclinical and clinical studies that investigate novel approaches or potential combination therapies to enhance the efficacy of pharmacological interventions in reducing neuroinflammation and associated neuroinflammatory diseases. In addition, carefully targeted reviews addressing the challenges faced in developing therapeutic agents that specifically target neuroinflammation without interfering with essential immune responses in the brain would also be highly valuable.

Dr. Xian (Phoebe) Zhou
Guest Editor

Manuscript Submission Information

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Keywords

  • neuroinflammation
  • pharmacological targets
  • microglia
  • astrocytes
  • cytokines
  • mechanism
  • novel approaches
  • combination therapy

Published Papers (2 papers)

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Research

21 pages, 4270 KiB  
Article
SGLT2 Inhibitor Canagliflozin Alleviates High Glucose-Induced Inflammatory Toxicity in BV-2 Microglia
by Ching-Tien Lee, Kun-Der Lin, Cheng-Fang Hsieh and Jiz-Yuh Wang
Biomedicines 2024, 12(1), 36; https://doi.org/10.3390/biomedicines12010036 - 22 Dec 2023
Viewed by 1189
Abstract
Patients with diabetes mellitus can experience hyperglycemia, which affects brain function and produces cognitive impairment or neurodegeneration. Neuroinflammation is an important cause of cognitive dysfunction. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are antihyperglycemic agents that reportedly possess anti-inflammatory properties and may produce beneficial cognitive [...] Read more.
Patients with diabetes mellitus can experience hyperglycemia, which affects brain function and produces cognitive impairment or neurodegeneration. Neuroinflammation is an important cause of cognitive dysfunction. Sodium-glucose cotransporter 2 (SGLT2) inhibitors are antihyperglycemic agents that reportedly possess anti-inflammatory properties and may produce beneficial cognitive effects. We hypothesized that SGLT2 inhibitors alleviate hyperglycemia-related inflammation in brain immune cells. Cultured BV-2 microglia were exposed to high glucose (HG) in the absence or presence of SGLT2 inhibitors including canagliflozin (Cana), dapagliflozin (Dapa), empagliflozin (Empa), and ertugliflozin (Ertu). Afterward, we evaluated the cytotoxic and inflammatory responses by specific biochemical assays. Treatments with non-toxic Cana or Dapa, but not Empa or Ertu, inhibited proliferation without cell death. Only Cana rescued BV-2 microglia from HG-induced cytotoxicity, including apoptosis or autophagic degradation. None of SGLT2 inhibitors affected the HG-stimulated induction of stress proteins HO-1 and HSP70. Also, compared to the other three SGLT2 inhibitors, Cana was better at inhibiting HG-induced oxidative/inflammatory stress, as evidenced by its ability to repress proinflammatory factors (e.g., oxygen free radicals, iNOS, NLRP3, IL-1β, and TNF-α) other than COX-2. Cana’s action to alleviate HG insults was mediated not by altering SGLT2 protein expression, but by reducing HG-stimulated signaling activities of NFκB, JNK, p38, and PI3K/Akt pathways. Particularly, Cana imitated the effects of NFκB inhibitor on HG-induced iNOS and COX-2. Of the four SGLT2 inhibitors, Cana provided BV-2 microglia with the best protection against HG-induced inflammatory toxicity. Thus, Cana may help to reduce innate neuroimmune damage caused by hyperglycemia. Full article
(This article belongs to the Special Issue Pharmacological Targets for Neuroinflammation)
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18 pages, 18809 KiB  
Article
Genes Involved by Dexamethasone in Prevention of Long-Term Memory Impairment Caused by Lipopolysaccharide-Induced Neuroinflammation
by Galina T. Shishkina, Tatyana S. Kalinina, Dmitriy A. Lanshakov, Veta V. Bulygina, Natalya P. Komysheva, Anita V. Bannova, Ulyana S. Drozd and Nikolay N. Dygalo
Biomedicines 2023, 11(10), 2595; https://doi.org/10.3390/biomedicines11102595 - 22 Sep 2023
Cited by 2 | Viewed by 1084
Abstract
Inflammatory activation within the brain is linked to a decrease in cognitive abilities; however, the molecular mechanisms implicated in the development of inflammatory-related cognitive dysfunction and its prevention are poorly understood. This study compared the responses of hippocampal transcriptomes 3 months after the [...] Read more.
Inflammatory activation within the brain is linked to a decrease in cognitive abilities; however, the molecular mechanisms implicated in the development of inflammatory-related cognitive dysfunction and its prevention are poorly understood. This study compared the responses of hippocampal transcriptomes 3 months after the striatal infusion of lipopolysaccharide (LPS; 30 µg), resulting in memory loss, or with dexamethasone (DEX; 5 mg/kg intraperitoneal) pretreatment, which abolished the long-term LPS-induced memory impairment. After LPS treatment, a significant elevation in the expression of immunity/inflammatory-linked genes, including chemokines (Cxcl13), cytokines (Il1b and Tnfsf13b), and major histocompatibility complex (MHC) class II members (Cd74, RT1-Ba, RT1-Bb, RT1-Da, and RT1-Db1) was observed. DEX pretreatment did not change the expression of these genes, but significantly affected the expression of genes encoding ion channels, primarily calcium and potassium channels, regulators of glutamate (Slc1a2, Grm5, Grin2a), and GABA (Gabrr2, Gabrb2) neurotransmission, which enriched in such GO biological processes as “Regulation of transmembrane transport”, “Cognition”, “Learning”, “Neurogenesis”, and “Nervous system development”. Taken together, these data suggest that (1) pretreatment with DEX did not markedly affect LPS-induced prolonged inflammatory response; (2) DEX pretreatment can affect processes associated with glutamatergic signaling and nervous system development, possibly involved in the recovery of memory impairment induced by LPS. Full article
(This article belongs to the Special Issue Pharmacological Targets for Neuroinflammation)
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