Evidence map›Paper›PMID 41057834›Full record

ArticleJournal of inflammation (London, England)2025

Baicalein inhibits mycobacterium tuberculosis-induced macrophage M1 polarization depending on the regulation of YY1/RAB10/TLR4 pathway.

Qing Zhou, Shuanghua Chen, Linfei Shu, Qian Wang, Ting Yuan, Yangjing Ou, Ling Qing, Xiaojin He

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of inflammation (London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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

8 authors.

Qing Zhou *Department of Infectious Diseases, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, No. 116, Changjiang South Road, Tianyuan District, Zhuzhou, 412007, China.
Shuanghua Chen *Hunan Traditional Chinese Medical College, Zhuzhou, China.
Linfei ShuDepartment of Urology Surgery, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, Zhuzhou, China.
Qian WangZhejiang ShengTing Biotech. Ltd, Taizhou, China.
Ting YuanDepartment of Infectious Diseases, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, No. 116, Changjiang South Road, Tianyuan District, Zhuzhou, 412007, China.
Yangjing OuDepartment of Infectious Diseases, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, No. 116, Changjiang South Road, Tianyuan District, Zhuzhou, 412007, China.
Ling QingDepartment of Infectious Diseases, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, No. 116, Changjiang South Road, Tianyuan District, Zhuzhou, 412007, China.
Xiaojin HeDepartment of Infectious Diseases, Zhuzhou Hospital Affiliated to Xiangya School of Medicine, Central South University, No. 116, Changjiang South Road, Tianyuan District, Zhuzhou, 412007, China. hxj597508286@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundBaicalein (Bai) has been found to alleviate the progression of tuberculosis (TB) by inhibiting mycobacterium tuberculosis (M.tb)-induced macrophage pyroptosis, so it may be used as an adjuvant treatment for TB. However, the underlying molecular mechanism of Bai remains unclear.

methodsTHP-1 macrophages were infected with M.tb and treated with Bai. The viability and apoptosis of macrophages were examined with CCK8 assay, flow cytometry and TUNEL staining. The levels of inflammatory cytokines were tested by ELISA. Macrophage M1 polarization was assessed by detecting CD86

resultsM.tb promoted macrophage M1 polarization, apoptosis and inflammation, while this effect was abolished by Bai treatment. Bai decreased RAB10 expression, and RAB10 overexpression reversed the anti-TB effect of Bai. YY1 enhanced the transcription of RAB10, and YY1 knockdown inhibited M.tb-induced macrophage M1 polarization by reducing RAB10 expression. Also, Bai could decrease YY1 expression, and YY1 overexpression eliminated the regulation of Bai on M.tb-induced macrophage M1 polarization. Moreover, RAB10 could interact with TLR4 to activate TLR4/MYD88/NF-κB pathway, thus promoting M.tb-induced macrophage M1 polarization.

conclusionBai might play anti-TB effect by regulating YY1/RAB10/TLR4/MYD88/NF-κB pathway, providing a novel idea for the treatment of TB.

Indexed as

BaicaleinMacrophagesMycobacterium tuberculosisTuberculosis

Identifiers

PMID41057834
PMCPMC12506312

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