Evidence map›Paper›PMID 37375642›Full record

ArticleNutrients2023

Taxifolin Suppresses Inflammatory Responses of High-Glucose-Stimulated Mouse Microglia by Attenuating the TXNIP-NLRP3 Axis.

Masayo Iwasa, Hisashi Kato, Kaori Iwashita, Hajime Yamakage, Sayaka Kato, Satoshi Saito, Masafumi Ihara, Hideo Nishimura, Atsuhiko Kawamoto, Takayoshi Suganami and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 25 citations in OpenAlex.

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  15. Role of microglia in diabetic neuropathic pain.Frontiers in cell and developmental biology · 2024
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Masayo IwasaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.
Hisashi KatoDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.ORCID 0000-0003-4395-8369
Kaori IwashitaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.
Hajime YamakageDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.
Sayaka KatoDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.
Satoshi SaitoDepartment of Neurology, National Cerebral and Cardiovascular Center, Osaka 564-8565, Japan.ORCID 0000-0001-8608-058X
Masafumi IharaDepartment of Neurology, National Cerebral and Cardiovascular Center, Osaka 564-8565, Japan.ORCID 0000-0002-7102-4048
Hideo NishimuraTranslational Research Center for Medical Innovation, Foundation for Biomedical Research and Innovation at Kobe, Kobe 650-0047, Japan.
Atsuhiko KawamotoTranslational Research Center for Medical Innovation, Foundation for Biomedical Research and Innovation at Kobe, Kobe 650-0047, Japan.
Takayoshi SuganamiDepartment of Molecular Medicine and Metabolism, Research Institute of Environmental Medicine, Nagoya University, Nagoya 464-8601, Japan.ORCID 0000-0002-1918-0465
Masashi TanakaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.ORCID 0000-0003-0719-8972
Noriko Satoh-AsaharaDepartment of Endocrinology, Metabolism and Hypertension Research, Clinical Research Institute, National Hospital Organization Kyoto Medical Center, Kyoto 612-8555, Japan.ORCID 0000-0002-8645-3144
Kyoto Medical Center · JPFoundation for Biomedical Research and Innovation · JPNational Cerebral and Cardiovascular Center · JPGifu University · JP

Funding

Health Science University N/AJapan Society for the Promotion of Science JP22K07411; JP22K11720; JP22K07456; JP21H02835; JP22K19723National Hospital Organization for collaborative clinical research H26-NHO-02
6 · The paper itself

Abstract

Type 2 diabetes mellitus is associated with an increased risk of dementia, potentially through multifactorial pathologies, including neuroinflammation. Therefore, there is a need to identify novel agents that can suppress neuroinflammation and prevent cognitive impairment in diabetes. In the present study, we demonstrated that a high-glucose (HG) environment elevates the intracellular reactive oxygen species (ROS) levels and triggers inflammatory responses in the mouse microglial cell line BV-2. We further found that thioredoxin-interacting protein (TXNIP), a ROS-responsive positive regulator of the nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, was also upregulated, followed by NLRP3 inflammasome activation and subsequent interleukin-1beta (IL-1β) production in these cells. Conversely, caspase-1 was not significantly activated, suggesting the involvement of noncanonical pathways in these inflammatory responses. Moreover, our results demonstrated that taxifolin, a natural flavonoid with antioxidant and radical scavenging activities, suppressed IL-1β production by reducing the intracellular ROS levels and inhibiting the activation of the TXNIP-NLRP3 axis. These findings suggest the novel anti-inflammatory effects of taxifolin on microglia in an HG environment, which could help develop novel strategies for suppressing neuroinflammation in diabetes.

Indexed as

Diabetes Mellitus, Type 2InflammasomesAnimalsGlucoseInterleukin-1betaMiceMicrogliaNeuroinflammatory DiseasesNLR Family, Pyrin Domain-Containing 3 ProteinQuercetinReactive Oxygen SpeciesGlucoseInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinQuercetinReactive Oxygen Speciestaxifolinantioxidanthigh glucoseinflammasomemicroglianeuroinflammationradical scavengertaxifolintype 2 diabetes mellitus

Identifiers

PMID37375642
PMCPMC10302635
OpenAlexW4380686313

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.