Evidence map›Paper›PMID 39543653›Full record

ArticleChinese medicine2024

Taraxerone inhibits M1 polarization and alleviates sepsis-induced acute lung injury by activating SIRT1.

Lang Deng, Weixi Xie, Miao Lin, Dayan Xiong, Lei Huang, Xiaohua Zhang, Rui Qian, Xiaoting Huang, Siyuan Tang, Wei Liu

Abstract read
In one paragraph

Article in Chinese medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
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  4. 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

10 authors.

Lang Deng *Xiangya Nursing School, Central South University, Changsha, 410013, Hunan, China.
Weixi Xie *Xiangya Nursing School, Central South University, Changsha, 410013, Hunan, China.
Miao LinXiangya Nursing School, Central South University, Changsha, 410013, Hunan, China.
Dayan XiongXiangya Nursing School, Central South University, Changsha, 410013, Hunan, China.
Lei HuangOccupational Disease Department, Hunan Prevention and Treatment Institute for Occupational Diseases, Changsha, 410021, Hunan, China.
Xiaohua ZhangOccupational Disease Department, Hunan Prevention and Treatment Institute for Occupational Diseases, Changsha, 410021, Hunan, China.
Rui QianXiangya Nursing School, Central South University, Changsha, 410013, Hunan, China.
Xiaoting HuangXiangya Nursing School, Central South University, Changsha, 410013, Hunan, China. huangxiaoting@csu.edu.cn.
Siyuan TangXiangya Nursing School, Central South University, Changsha, 410013, Hunan, China. sytang263@csu.edu.cn.
Wei LiuXiangya Nursing School, Central South University, Changsha, 410013, Hunan, China. liuw079@csu.edu.cn.ORCID http://orcid.org/0000-0003-0948-7807

Funding

Fundamental Research Funds for Central Universities of the Central South University 2023ZZTS0862Fundamental Research Funds for the Central Universities of Central South University CX20210344National Key Research and Development Program of China 2022YFC3601603National Natural Science Foundation of China 81500056National Natural Science Foundation of China 82100084National Natural Science Foundation of China 82170853Natural Science Foundation of Hunan Province 2016JJ3182Natural Science Foundation of Hunan Province 2020JJ4773Natural Science Foundation of Hunan Province 2021JJ30899the Fund for the State Key Laboratory of Hunan Province 2017TP1004the open Sharing Fund for the Large-scale Instruments and Equipment of Central South University CSUZC202251the science and technology innovation program of Hunan province 2022WZ1033
6 · The paper itself

Abstract

backgroundAcute lung injury (ALI) is the most lethal disease associated with sepsis, and there is a lack of effective drug treatment. As the major cells of sepsis-induced ALI, macrophages polarize toward the proinflammatory M1 phenotype and secrete multiple inflammatory cytokines to accelerate the disease process through nuclear factor kappa-B (NF-κB) and NLR family pyrin domain containing 3 (NLRP3) inflammasome signaling pathways. Taraxerone, the main component of the Chinese medicinal Sedum, possesses numerous biological activities. However, uncertainty remains regarding the potential of taraxerone to protect against sepsis-induced ALI. This study aimed to investigate the effects and mechanisms of taraxerone against ALI.

methodsAn animal model for ALI was established by cecal ligation and puncture and treated with taraxerone via intraperitoneal administration. The protective effect of taraxerone on the lungs was analyzed using H&E staining, dihydroethidium staining, ELISA kits, cell counting, myeloperoxidase kit, malondialdehyde kit, glutathione kit, superoxide dismutase kit and flow cytometry. Western blotting, RT-PCR, flow cytometry, co-immunoprecipitation, and immunofluorescence were used to investigate the regulatory of taraxerone on SIRT1.

resultsOur study demonstrates for the first time that taraxerone can activate SIRT1 in macrophages, promoting SIRT1 activity. This activation inhibited the NF-κB signaling pathway primarily through the dephosphorylation and deacetylation of p65. Simultaneously, taraxerone disrupted the NLRP3 inflammasome signaling pathway, thereby alleviating M1 polarization of macrophages and mitigating sepsis-induced pulmonary inflammation and oxidative stress. In vivo, EX527 was used to validate the anti-inflammatory and anti-oxidative stress effects of taraxerone mediated by SIRT1.

conclusionSIRT1-mediated anti-inflammatory and anti-oxidative stress effects may be important targets for taraxerone in treating ALI.

Indexed as

Acute lung injuryInflammationMacrophage polarizationOxidative stressSIRT1Taraxerone

Identifiers

PMID39543653
PMCPMC11566926

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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.