Evidence map›Paper›PMID 32457419›Full record

ArticleActa pharmacologica Sinica2021

Baicalin prevents LPS-induced activation of TLR4/NF-κB p65 pathway and inflammation in mice via inhibiting the expression of CD14.

Ya-Jun Fu, Bo Xu, Shao-Wei Huang, Xia Luo, Xiang-Liang Deng, Shuang Luo, Chang Liu, Qing Wang, Jin-Yan Chen, Lian Zhou

Open access · bronzeAbstract read
In one paragraph

Article in Acta pharmacologica Sinica, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
126citing papers in PubMed, 2 pooled it
5.2field-weighted citation impact, top 3% 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

126 citing papers in PubMed, 2 syntheses or guidelines pooled it, 212 citations in OpenAlex.

  1. Pooled it
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66 more citing papers are in PubMed but not listed here.

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

10 authors at 1 institution in 1 country.

Ya-Jun FuSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Bo XuSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Shao-Wei HuangSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Xia LuoSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Xiang-Liang DengSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. dxl@gdpu.edu.cn.
Shuang LuoSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Chang LiuSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Qing WangSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Jin-Yan ChenSchool of Basic Medical Science, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China.
Lian ZhouSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, China. zl@gzucm.edu.cn.
Guangzhou University of Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that baicalin, an active ingredient of the Chinese traditional medicine Huangqin, attenuates LPS-induced inflammation by inhibiting the activation of TLR4/NF-κBp65 pathway, but how it affects this pathway is unknown. It has been shown that CD14 binds directly to LPS and plays an important role in sensitizing the cells to minute quantities of LPS via chaperoning LPS molecules to the TLR4/MD-2 signaling complex. In the present study we investigated the role of CD14 in the anti-inflammatory effects of baicalin in vitro and in vivo. Exposure to LPS (1 μg/mL) induced inflammatory responses in RAW264.7 cells, evidenced by marked increases in the expression of MHC II molecules and the secretion of NO and IL-6, and by activation of MyD88/NF-κB p65 signaling pathway, as well as the expression of CD14 and TLR4. These changes were dose-dependently attenuated by pretreatment baicalin (12.5-50 μM), but not by baicalin post-treatment. In RAW264.7 cells without LPS stimulation, baicalin dose-dependently inhibit the protein and mRNA expression of CD14, but not TLR4. In RAW264.7 cells with CD14 knockdown, baicalin pretreatment did not prevent inflammatory responses and activation of MyD88/NF-κB p65 pathway induced by high concentrations (1000 μg/mL) of LPS. Furthermore, baicalin pretreatment also inhibited the expression of CD14 and activation of MyD88/NF-κB p65 pathway in LPS-induced hepatocyte-derived HepG2 cells and intestinal epithelial-derived HT-29 cells. In mice with intraperitoneal injection of LPS and in DSS-induced UC mice, oral administration of baicalin exerted protective effects by inhibition of CD14 expression and inflammation. Taken together, we demonstrate that baicalin pretreatment prevents LPS-induced inflammation in RAW264.7 cells in CD14-dependent manner. This study supports the therapeutic use of baicalin in preventing the progression of LPS-induced inflammatory diseases.

Indexed as

AnimalsAnti-Inflammatory AgentsCell Line, TumorFlavonoidsGene Knockdown TechniquesHumansInflammationLipopolysaccharide ReceptorsLipopolysaccharidesMaleMiceMice, Inbred BALB CMice, Inbred C57BLMyeloid Differentiation Factor 88Protective AgentsRAW 264.7 CellsAnti-Inflammatory AgentsbaicalinCd14 protein, mouseFlavonoidsLipopolysaccharide ReceptorsLipopolysaccharidesMYD88 protein, humanMyeloid Differentiation Factor 88Protective AgentsRELA protein, humanRela protein, mouseTlr4 protein, mouseToll-Like Receptor 4Transcription Factor RelAbaicalinCD14inflammatory diseasesNF-κB p65RAW264.7 cellsTLR4

Identifiers

PMID32457419
PMCPMC7921675
OpenAlexW3031572820

What OpenQuestion holds

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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.