Evidence map›Paper›PMID 28577049›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2017

Eburicoic acid from Laetiporus sulphureus (Bull.:Fr.) Murrill attenuates inflammatory responses through inhibiting LPS-induced activation of PI3K/Akt/mTOR/NF-κB pathways in RAW264.7 cells.

Junzhi Wang, Pan Zhang, Haibo He, Xinxin Se, Wenjun Sun, Beiyan Chen, Lin Zhang, Ximing Yan, Kun Zou

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.5field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. TheAnimals : an open access journal from MDPI · 2021
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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

9 authors at 1 institution in 1 country.

Junzhi WangHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
Pan ZhangHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
Haibo HeHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China. hehaibo252219@163.com.
Xinxin SeHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
Wenjun SunHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
Beiyan ChenHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
Lin ZhangHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
Ximing YanHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
Kun ZouHubei Key Laboratory of Natural Products Research and Development, College of Biological and Pharmaceutical Science, China Three Gorges University, Yichang, Hubei, 443002, China.
China Three Gorges University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Excessive activation of macrophages has been implicated in various types of inflammatory injury. Suppression of macrophage activation would have therapeutic benefits, leading to the alleviation of the progression of inflammatory diseases. Eburicoic acid (EA) is one of main bioactive components isolated from Laetiporus sulphureus (Bull.:Fr.) Murrill. In our previous study, we found that EA possessed anti-inflammatory activities. However, the cellular and molecular mechanisms underlying its anti-inflammatory activities remain to be poorly understood. The present study aimed to further evaluate its effect on lipopolysaccharide (LPS)-induced inflammatory responses in RAW264.7 macrophage cells. We investigated the anti-inflammatory effect by modulating LPS-induced activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR)/nuclear transcription factor-κB (NF-κB) pathway in RAW264.7 cells. The results showed that EA caused no obvious cytotoxicity, and its suitable concentrations on RAW264.7 cells were in the range from 0.02 to 0.08 μM. EA significantly inhibited the releases of inflammatory mediators, nitrite oxide (NO) and prostaglandin E2 (PGE

Indexed as

AnimalsAnti-Inflammatory AgentsCell SurvivalCyclooxygenase 2CytokinesDinoprostoneLanosterolLipopolysaccharidesMiceNitric OxideNitric Oxide Synthase Type IIPhosphatidylinositol 3-KinasePolyporalesProto-Oncogene Proteins c-aktRAW 264.7 CellsSignal TransductionAnti-Inflammatory AgentsCyclooxygenase 2CytokinesDinoprostoneeburicoic acidLanosterolLipopolysaccharidesmTOR protein, mouseNitric OxideNitric Oxide Synthase Type IINos2 protein, mousePhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktPtgs2 protein, mouseTOR Serine-Threonine KinasesTranscription Factor RelAEburicoic acidInflammatory mediatorsPI3K/Akt/mTOR/NF-κB signaling pathwayPro-inflammatory cytokinesRAW264.7 cells

Identifiers

PMID28577049
OpenAlexW2620726669

What OpenQuestion holds

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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.