Evidence map›Paper›PMID 35974091›Full record

ArticleScientific reports2022

Salvianolic acid B inhibits RAW264.7 cell polarization towards the M1 phenotype by inhibiting NF-κB and Akt/mTOR pathway activation.

Tao Zou, Shan Gao, Zhaolan Yu, Fuyong Zhang, Lan Yao, Mengyao Xu, Junxin Li, Zhigui Wu, Yilan Huang, Shurong Wang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
2.2field-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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
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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

10 authors at 2 institutions in 1 country.

Tao Zou *Department of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Shan Gao *Department of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Zhaolan YuDepartment of Nephrology, The Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Fuyong ZhangDepartment of Pharmacy, People's Hospital of Deyang City, Deyang, 618000, China.
Lan YaoDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Mengyao XuDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Junxin LiDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Zhigui WuDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China.
Yilan HuangDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. hyl3160131@163.com.
Shurong WangDepartment of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou, 646000, China. wangshurong011@swmu.edu.cn.
Affiliated Hospital of Southwest Medical University · CNSouthwest Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

M1 macrophages secrete a large number of proinflammatory factors and promote the expansion of atherosclerotic plaques and processes. Salvianolic acid B (Sal B) exerts anti-inflammatory, antitumor and other effects, but no study has addressed whether Sal B can regulate the polarization of macrophages to exert these anti-atherosclerotic effects. Therefore, we investigated the inhibition of Sal B in M1 macrophage polarization and the underlying mechanism. The effects of different treatments on cell viability, gene expression and secretion of related proteins, phenotypic markers and cytokines were detected by MTT and western blot assays, RT‒qPCR and ELISAs. Cell viability was not significantly changed when the concentration of Sal B was less than 200 μM, and Lipopolysaccharide (LPS) (100 ng/mL) + interferon-γ (IFN-γ) (2.5 ng/mL) successfully induced M1 polarization. RT‒qPCR and ELISAs indicated that Sal B can downregulate M1 marker (Inducible Nitric Oxide Synthase (iNOS), Tumor Necrosis Factor-α (TNF-α), and Interleukin-6 (IL-6)) and upregulate M2 marker (Arginase-1 (Arg-1) and Interleukin-10 (IL-10)) expression. Western blotting was performed to measure the expression of Nuclear Factor-κB (NF-κB), p-Akt, p-mTOR, LC3-II, Beclin-1, and p62, and the results suggested that Sal B inhibits the M1 polarization of RAW264.7 macrophages by promoting autophagy via the NF-κB signalling pathway. The study indicated that Sal B inhibits M1 macrophage polarization by inhibiting NF-κB signalling pathway activation and downregulating Akt/mTOR activation to promote autophagy.

Indexed as

NF-kappa BProto-Oncogene Proteins c-aktAnimalsBenzofuransDepsidesLipopolysaccharidesMicePhenotypeRAW 264.7 CellsTOR Serine-Threonine KinasesBenzofuransDepsidesLipopolysaccharidesNF-kappa BProto-Oncogene Proteins c-aktsalvianolic acid BTOR Serine-Threonine Kinases

Identifiers

PMID35974091
PMCPMC9381594
OpenAlexW4292181519

What OpenQuestion holds

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LicenceCC BY
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.