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Biomedicines
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Pharmacological Targets for Neuroinflammation
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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: closed (31 July 2024) | Viewed by 6571

Special Issue Editor

Dr. Xian (Phoebe) Zhou

E-Mail Website
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

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Published Papers (5 papers)

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Research

Jump to: Review

18 pages, 3217 KiB  
Article
BV2 Microglial Cell Activation/Polarization Is Influenced by Extracellular Vesicles Released from Mutated SOD1 NSC-34 Motoneuron-like Cells
by Elisabetta Carata, Marco Muci, Stefania Mariano and Elisa Panzarini
Biomedicines 2024, 12(9), 2069; https://doi.org/10.3390/biomedicines12092069 - 11 Sep 2024
Viewed by 358
Abstract
Microglia-mediated neuroinflammation is a key player in the pathogenesis of amyotrophic lateral sclerosis (ALS) as it can contribute to the progressive degeneration of motor neurons (MNs). Here, we investigated the role of mSOD1 NSC-34 MN-like cell-derived extracellular vesicles (EVs) in inducing the activation [...] Read more.
Microglia-mediated neuroinflammation is a key player in the pathogenesis of amyotrophic lateral sclerosis (ALS) as it can contribute to the progressive degeneration of motor neurons (MNs). Here, we investigated the role of mSOD1 NSC-34 MN-like cell-derived extracellular vesicles (EVs) in inducing the activation of BV2 microglial cells. NSC-34-released EVs were isolated by culture medium differential ultracentrifugation to obtain two fractions, one containing small EVs (diameter < 200 nm) and the other containing large EVs (diameter > 200 nm). BV2 cells were incubated with the two EV fractions for 12, 24, and 48 h to evaluate 1) the state of microglial inflammation through RT-PCR of IL-1β, IL-6, IL-4, and IL-10 and 2) the expression of proteins involved in inflammasome activation (IL-β and caspase 1), cell death (caspase 3), and glial cell recruitment (CXCR1), and presence of the TGFβ cytokine receptor (TGFβ-R2). The obtained results suggest a mSOD1 type-dependent polarization of BV2 cells towards an early neurotoxic phenotype and a late neuroprotective status, with an appearance of mixed M1 and M2 microglia subpopulations. A significant role in driving microglial cell activation is played by the TGFβ/CX3CR1 axis. Therefore, targeting the dysregulated microglial response and modulating neuroinflammation could hold promise as a therapeutic strategy for ALS. Full article
(This article belongs to the Special Issue Pharmacological Targets for Neuroinflammation)
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15 pages, 2099 KiB  
Article
Evaluation of Neuroinflammatory Contribution to Neurodegeneration in LRRK2 Drosophila Models
by Hoai Nam Nguyen, Grazia Galleri, Antonio Rassu, Cristina Ciampelli, Roberto Bernardoni, Manuela Galioto, Diego Albani, Claudia Crosio and Ciro Iaccarino
Biomedicines 2024, 12(7), 1555; https://doi.org/10.3390/biomedicines12071555 - 12 Jul 2024
Viewed by 695
Abstract
Pathological mutations in the LRRK2 gene are the major genetic cause of Parkinson’s disease (PD). Although several animal models with either LRRK2 down- or over-expression have been developed, the physiological function of LRRK2 remains elusive. LRRK2 is constitutively expressed in various tissues including [...] Read more.
Pathological mutations in the LRRK2 gene are the major genetic cause of Parkinson’s disease (PD). Although several animal models with either LRRK2 down- or over-expression have been developed, the physiological function of LRRK2 remains elusive. LRRK2 is constitutively expressed in various tissues including neurons and glial cells, but importantly, it is expressed at low levels in dopaminergic neurons, further contributing to the cryptic function of LRRK2. Significant levels of LRRK2 protein and mRNA have been detected in peripheral blood mononuclear cells, lymph nodes, the spleen, and primary microglia, strongly suggesting the contribution of inflammatory cells to neuronal degeneration. In this research article, using Drosophila LRRK2 models, we were able to demonstrate a significant contribution of glial cells to the LRRK2 pathological phenotype. Furthermore, in Drosophila, neurodegeneration is associated with a significant and important increase in specific inflammatory peptides. Finally, levetiracetam, a compound widely used in human therapy to treat epilepsy, was able to rescue both neuronal degeneration and neuroinflammation. Full article
(This article belongs to the Special Issue Pharmacological Targets for Neuroinflammation)
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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
Cited by 4 | Viewed by 1690
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 3 | Viewed by 1396
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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Review

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22 pages, 932 KiB  
Review
Combination Therapy for Sustainable Fish Oil Products: Improving Cognitive Function with n-3 PUFA and Natural Ingredients
by Anthony Arsecularatne, Rotina Kapini, Yang Liu, Dennis Chang, Gerald Münch and Xian Zhou
Biomedicines 2024, 12(6), 1237; https://doi.org/10.3390/biomedicines12061237 - 3 Jun 2024
Viewed by 1231
Abstract
Long-chain polyunsaturated omega-3 fatty acids (n-3 PUFAs), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are recommended as beneficial dietary supplements for enhancing cognitive function. Although fish oil (FO) is renowned for its abundant n-3 PUFA content, combining FO with other natural products [...] Read more.
Long-chain polyunsaturated omega-3 fatty acids (n-3 PUFAs), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), are recommended as beneficial dietary supplements for enhancing cognitive function. Although fish oil (FO) is renowned for its abundant n-3 PUFA content, combining FO with other natural products is considered as a viable option to support the sustainable development of FO products. This review aims to provide comprehensive insights into the advanced effects of combining FO or its components of DHA and EPA with natural products on protecting cognitive function. In two double-blind random control trials, no advanced effects were observed for adding curcumin to FO on cerebral function protection. However, 16 week’s treatment of FO combined with vitamin E did not yield any advanced effects in cognitive factor scores. Several preclinical studies have demonstrated that combinations of FO with natural products can exhibit advanced effects in addressing pathological components in cognitive impairment, including neuroinflammation, oxidative stress, and neuronal survival. In conclusion, evidence from clinical trials for beneficial use of FO and natural ingredients combination is lacking. Greater cohesion is needed between preclinical and clinical data to substantiate the efficacy of FO and natural product combinations in preventing or slowing the progression of cognitive decline. Full article
(This article belongs to the Special Issue Pharmacological Targets for Neuroinflammation)
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