Naringenin promotes microglial M2 polarization and Aβ degradation enzyme expression

@article{Yang2019NaringeninPM,
  title={Naringenin promotes microglial M2 polarization and A$\beta$ degradation enzyme expression},
  author={Zhiyou Yang and Tomoharu Kuboyama and Chihiro Tohda},
  journal={Phytotherapy Research},
  year={2019},
  volume={33},
  pages={1114 - 1121}
}
Two kinds of microglia are known, classical M1 and alternative M2 phenotypes. Amyloid β (Aβ), a critical cause of Alzheimer's disease (AD), promotes M1 microglial polarization, leading to neuroinflammation and neuronal death. M2 microglia play important roles in anti‐inflammatory effects, Aβ clearance, and memory recovery in AD. Therefore, increasing of M2 microglia is expected to recover from AD. We previously found that naringenin, a blood–brain barrier penetrating compound, decreased A… 
View on Wiley
ncbi.nlm.nih.gov
27 Citations
Highly Influential Citations
1
Background Citations
10
Methods Citations
3

27 Citations

Citation Type

Citation Type

Hederagenin Modulates M1 Microglial Inflammatory Responses and Neurite Outgrowth
TLDR
Hederagenin (HED), a naturally occurring triterpene compound, inhibited lipopolysaccharide-induced nitric oxide generation and downregulated expression of proinflammatory cytokines, such as tumor necrosis factor-α, interleukin-1 β (IL-1β), and IL-6, and might be a therapeutic candidate for AD.
Platycodigenin as Potential Drug Candidate for Alzheimer’s Disease via Modulating Microglial Polarization and Neurite Regeneration
TLDR
This study clarified that platycodigenin effectively ameliorated LPS-induced inflammation and Aβ-induced neurite atrophy and neuronal death and promoted neurite regeneration and neuronal survival after Aβ treatment in primary cortical neurons.
KRIBB11: A Promising Drug that Promotes Microglial Process Elongation and Suppresses Neuroinflammation
TLDR
It is demonstrated that KRIBB11 is a novel compound that can prevent microglial activation and neuroinflammation-associated behavioral deficits possibly through inducing the Akt-mediated elongation of microglia process.
Naringenin Upregulates AMPK-Mediated Autophagy to Rescue Neuronal Cells From β-Amyloid (1–42) Evoked Neurotoxicity
TLDR
Naringenin in silico exhibits a robust affinity with AMP-activated protein kinase (AMPK) and upregulated AMPK-mediated autophagy signaling in neurons, which led to the protection against Aβ1–42 evoked neurotoxicity and highlights the neuroprotective potential of naringen in that can be developed as an anti-amyloidogenic nutraceutical.
Heterogeneity of Microglia Phenotypes: Developmental, Functional and Some Therapeutic Considerations.
TLDR
Proper therapeutic designs including the use of anti-inflammatory drugs, herbal agents may be beneficial in suppression of microglial activation, especially M1 phenotype, for amelioration of neuroinflammation in different neuropathological conditions.
Mechanisms Involved in Microglial-Interceded Alzheimer’s Disease and Nanocarrier-Based Treatment Approaches
TLDR
As a targeted drug delivery system, nanocarrier approaches could emerge as a novel means to overcome existing AD therapy limitations and become an emerging target for managing and treating AD.
Neuroprotective effect of tormentic acid against memory impairment and neuro-inflammation in an Alzheimer's disease mouse model
TLDR
It is suggested that TA could attenuate neuro-inflammation and memory impairment, which may be closely associated with regulation of the NF-κB pathway.
A novel rhamnoside derivative PL402 up-regulates matrix metalloproteinase 3/9 to promote Aβ degradation and alleviates Alzheimer’s-like pathology
TLDR
This study demonstrates a rhamnoside derivative PL402 suppressed Aβ level in cell models without changing the expression or activity of Aβ generation-related secretases and suggests that PL402 may reduce Aβ via MMP3/9-mediated Aβ degradation.
New insights in drug development for Alzheimer's disease based on microglia function.
Disease Stage-Associated Alterations in Learning and Memory through the Electroacupuncture Modulation of the Cortical Microglial M1/M2 Polarization in Mice with Alzheimer's Disease
TLDR
It is proposed that electroacupuncture at the Shenting and Baihui acupoints could regulate microglial polarization and decrease Aβ plaques to improve learning and memory in mild AD mice.
...
...

References

SHOWING 1-10 OF 36 REFERENCES
M2 Macrophage Transplantation Ameliorates Cognitive Dysfunction in Amyloid-β-Treated Rats Through Regulation of Microglial Polarization.
TLDR
M2 macrophage transplantation attenuated inflammation in the brain, reversed Aβ1 - 42-induced changes in the IRF4-IRF5 ratio, drove endogenous microglial polarization toward the M2 phenotype, and ameliorated cognitive impairment.
Differential Roles of M1 and M2 Microglia in Neurodegenerative Diseases
TLDR
The changes of microglial phenotypes depend on the disease stages and severity; mastering the stage-specific switching of M1/M2 phenotypes within appropriate time windows may provide better therapeutic benefit.
Naringenin Suppresses Neuroinflammatory Responses Through Inducing Suppressor of Cytokine Signaling 3 Expression
TLDR
The findings suggest that naringenin-inhibited iNOS and COX-2 expression is mediated by SOCS-3 activation through AMPKα and PKCδ signaling pathways.
Arginase 1+ microglia reduce Aβ plaque deposition during IL-1β-dependent neuroinflammation
TLDR
It is suggested that Arg1+ microglia are involved in Aβ plaque reduction during sustained, IL-1β-dependent neuroinflammation, opening up possible new avenues for immunomodulatory therapy of AD.
Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer's disease
Compelling evidence from basic molecular biology has demonstrated the dual roles of microglia in the pathogenesis of Alzheimer's disease (AD). On one hand, microglia are involved in AD pathogenesis…
Microglial Phagocytosis Induced by Fibrillar β-Amyloid and IgGs Are Differentially Regulated by Proinflammatory Cytokines
TLDR
It is reported that proinflammatory cytokines attenuate microglial phagocytosis stimulated by fA β or complement receptor 3 and argued that this may, in part, underlie the accumulation of fAβ-containing plaques within the AD brain.
Dihydromyricetin inhibits microglial activation and neuroinflammation by suppressing NLRP3 inflammasome activation in APP/PS1 transgenic mice
TLDR
Whether Dihydromyricetin (DHM), a plant flavonoid compound, is effective therapies for AD is assessed; it is crucial to know whether DHM will affect microglial activation and neuroinflammation in APP/PS1 transgenic mice.
Mechanisms of Aβ Clearance and Degradation by Glial Cells
TLDR
The mechanisms of Aβ degradation by glial cells include the production of proteases, including neprilysin, the insulin degrading enzyme, and the endothelin-converting enzymes, able to hydrolyse Aβ at different cleavage sites.
IL-4-Induced Selective Clearance of Oligomeric β-Amyloid Peptide1–42 by Rat Primary Type 2 Microglia1
TLDR
IL-4-stimulated uptake and degradation of o-Aβ1–42 were selectively enhanced in type 2, but not type 1 MG that express CD40, which suggests that the two MG types may play different neuroimmunomodulating roles in the Aβ-overproducing brain.
Microglial Aβ Receptors in Alzheimer’s Disease
  • Yang Yu, R. Ye
  • Biology
    Cellular and Molecular Neurobiology
  • 2014
TLDR
This review focuses on microglial membrane receptors that bind Aβ and contribute to microglia activation and/or Aβ phagocytosis and clearance and the potential therapeutic value of these receptors in AD.
...
...