Evidence map›Paper›PMID 35017318›Full record

ArticleAging2022

Atorvastatin suppresses NLRP3 inflammasome activation in intracerebral hemorrhage via TLR4- and MyD88-dependent pathways.

Duo Chen, Lu Sui, Cao Chen, Sanchuan Liu, Xianfeng Sun, Junhong Guan

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

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 29 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Duo ChenDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, PR China.
Lu SuiDepartment of Pathophysiology, Shenyang Medical College, Shenyang 110034, PR China.
Cao ChenDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, PR China.
Sanchuan LiuDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, PR China.
Xianfeng SunDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, PR China.
Junhong GuanDepartment of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, PR China.
China Medical University · CNShenyang Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intracerebral hemorrhage (ICH) is a common neurological condition that causes severe disability and even death. Even though the mechanism is not clear, increasing evidence shows the efficacy of atorvastatin on treating ICH. In this study, we examined the impact of atorvastatin on the NOD-like receptor protein 3 (NLRP3) inflammasome and inflammatory pathways following ICH. Mouse models of ICH were established by collagenase injection in adult C57BL/6 mice. IHC mice received atorvastatin treatment 2 h after hematoma establishment. First, the changes of glial cells and neurons in the brains of ICH patients and mice were detected by immunohistochemistry and western blotting. Second, the molecular mechanisms underlying the microglial activation and neuronal loss were evaluated after the application of atorvastatin. Finally, the behavioral deficits of ICH mice without or with the treatment of atorvastatin were determined by neurological defect scores. The results demonstrated that atorvastatin significantly deactivated glial cells by reducing the expression of glial fibrillary acidic protein (GFAP), Ionized calcium binding adapter molecule 1 (Iba1), tumor necrosis factor (TNF)-α, and interleukin (IL)-6 in ICH model mice. For inflammasomes, atorvastatin also showed its efficacy by decreasing the expression of NLRP3, cleaved caspase-1, and IL-1β in ICH mice. Moreover, atorvastatin markedly inhibited the upregulation of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88), which indicated deactivation of NLRP3 inflammasomes. By inhibiting the activities of inflammasomes in glial cells, neuronal loss was partially prevented by suppressing the apoptosis in the brains of ICH mice, protecting them from neurological defects.

Indexed as

AnimalsAtorvastatinCerebral HemorrhageCytokinesGene Expression RegulationHumansHydroxymethylglutaryl-CoA Reductase InhibitorsInflammationMaleMiceMice, Inbred C57BLMyeloid Differentiation Factor 88NeuronsNLR Family, Pyrin Domain-Containing 3 ProteinSignal TransductionToll-Like Receptor 4AtorvastatinCytokinesHydroxymethylglutaryl-CoA Reductase InhibitorsMYD88 protein, humanMyd88 protein, mouseMyeloid Differentiation Factor 88NLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanNlrp3 protein, mouseTLR4 protein, humanTlr4 protein, mouseToll-Like Receptor 4atorvastatinintracerebral hemorrhageneuronal lossNLRP3 inflammasometoll-like receptor 4

Identifiers

PMID35017318
PMCPMC8791214
OpenAlexW4205987839

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.