Evidence map›Paper›PMID 26754542›Full record

ArticleCellular and molecular neurobiology2016

Hydroxysafflor Yellow A Attenuates Neuron Damage by Suppressing the Lipopolysaccharide-Induced TLR4 Pathway in Activated Microglial Cells.

Yanni Lv, Yisong Qian, Aijun Ou-Yang, Longsheng Fu

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 38 citations in OpenAlex.

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  17. Hydroxysafflor Yellow A: A Promising Therapeutic Agent for a Broad Spectrum of Diseases.Evidence-based complementary and alternative medicine : eCAM · 2018
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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

4 authors at 2 institutions in 1 country.

Yanni LvPharmacy Department, The First Affiliated Hospital of Nanchang University, Yongwai Street 17, Nanchang, 330006, China. lvyanni@126.com.
Yisong QianInstitute of Translational Medicine, Nanchang University, Nanchang, 330001, China.
Aijun Ou-YangPharmacy Department, The First Affiliated Hospital of Nanchang University, Yongwai Street 17, Nanchang, 330006, China.
Longsheng FuPharmacy Department, The First Affiliated Hospital of Nanchang University, Yongwai Street 17, Nanchang, 330006, China.
First Affiliated Hospital of Nanchang University · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Microglia activation initiates a neurological deficit cascade that contributes to substantial neuronal damage and impairment following ischemia stroke. Toll-like receptor 4 (TLR4) has been demonstrated to play a critical role in this cascade. In the current study, we tested the hypothesis that hydroxysafflor yellow A (HSYA), an active ingredient extracted from Flos Carthami tinctorii, alleviated inflammatory damage, and mediated neurotrophic effects in neurons by inducing the TLR4 pathway in microglia. A non-contact Transwell co-culture system comprised microglia and neurons was treated with HSYA followed by a 1 mg/mL lipopolysaccharide (LPS) stimulation. The microglia were activated prior to neuronal apoptosis, which were induced by increasing TLR4 expression in the activated microglia. However, HSYA suppressed TLR4 expression in the activated microglia, resulting in less neuronal damage at the early stage of LPS stimulation. Western blot analysis and immunofluorescence indicated that dose-dependently HSYA down-regulated TLR4-induced downstream effectors myeloid differentiation factor 88 (MyD88), nuclear factor kappa b (NF-κB), and the mitogen-activated protein kinases (MAPK)-regulated proteins c-Jun NH2-terminal protein kinase (JNK), protein kinase (ERK) 1/2 (ERK1/2), p38 MAPK (p38), as well as the LPS-induced inflammatory cytokine release. However, HSYA up-regulated brain-derived neurotrophic factor (BDNF) expression. Our data suggest that HSYA could exert neurotrophic and anti-inflammatory functions in response to LPS stimulation by inhibiting TLR4 pathway-mediated signaling.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCaspase 3ChalconeCoculture TechniquesCytokinesDown-RegulationFemaleLipopolysaccharidesMiceMicrogliaMyeloid Differentiation Factor 88NeuronsNeuroprotective AgentsPregnancyProtein TransportBrain-Derived Neurotrophic FactorCasp3 protein, mouseCaspase 3ChalconeCytokineshydroxysafflor yellow ALipopolysaccharidesMyd88 protein, mouseMyeloid Differentiation Factor 88Neuroprotective AgentsQuinonesRela protein, mouseTlr4 protein, mouseToll-Like Receptor 4Transcription Factor RelAAnti-inflammatoryCo-culture systemHydroxysafflor yellow AMicrogliaNeuronsNeuroprotective effectNeurotrophicToll-like receptor 4

Identifiers

PMID26754542
PMCPMC11482422
OpenAlexW2268173872

What OpenQuestion holds

Textmetadata
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.