Evidence map›Paper›PMID 34806444›Full record

ArticleInnate immunity2021

Chrysosplenol D protects mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via TLR4-MAPKs/NF-κB signaling pathways.

Qinqin Zhang, Aozi Feng, Mengnan Zeng, Beibei Zhang, Jingya Shi, Yaxin Lv, Bing Cao, Chenxin Zhao, Mengya Wang, Yifan Ding and 1 more

Open access · goldAbstract read
In one paragraph

Article in Innate immunity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  12. Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023
    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

11 authors at 3 institutions in 1 country.

Qinqin Zhang232830Henan University of Chinese Medicine, Zhengzhou, China.
Aozi FengDepartment of Clinical Research, the First Affiliated Hospital of Jinan University, Guangzhou, China.
Mengnan Zeng232830Henan University of Chinese Medicine, Zhengzhou, China.
Beibei Zhang232830Henan University of Chinese Medicine, Zhengzhou, China.
Jingya Shi232830Henan University of Chinese Medicine, Zhengzhou, China.
Yaxin Lv232830Henan University of Chinese Medicine, Zhengzhou, China.
Bing Cao232830Henan University of Chinese Medicine, Zhengzhou, China.
Chenxin Zhao232830Henan University of Chinese Medicine, Zhengzhou, China.
Mengya Wang232830Henan University of Chinese Medicine, Zhengzhou, China.
Yifan Ding232830Henan University of Chinese Medicine, Zhengzhou, China.
Xiaoke Zheng232830Henan University of Chinese Medicine, Zhengzhou, China.ORCID 0000-0003-3671-231X
Henan Bioengineering Technology Research Center · CNFirst Affiliated Hospital of Henan University · CNFirst Affiliated Hospital of Jinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study investigated the effect and mechanism of chrysosplenol D (CD) on LPS-induced acute lung injury in mice. Histological changes in the lungs were measured by hematoxylin-eosin staining. The levels of IL-6, IL-1β, and TNF-α in the bronchoalveolar lavage fluid were detected by ELISA. The levels of oxidative stress were detected by the cuvette assay. Immune cells in peripheral blood, the levels of reactive oxygen species, and apoptosis of primary lung cells were detected by flow cytometry. The mRNA levels of TLR4, MyD88, IL-1β, and NLRP3 were measured by quantitative real-time polymerase chain reaction. The levels of proteins in apoptosis and the TLR4-MAPKs/NF-κB signaling pathways were detected by Western blot. Hematoxylin-eosin staining showed that CD could improve lung injury; decrease the levels of inflammatory factors, oxidative stress, reactive oxygen species, and cell apoptosis; and regulate the immune system. Moreover, CD could down-regulate the mRNA levels of TLR4, MyD88, NLRP3, and IL-1β in lung, and the protein levels of Keap-1, Cleaved-Caspase-3/Caspase-3, Cleaved-Caspase-9/Caspase-9, TLR4, MyD88, p-ERK/ERK, p-JNK/JNK, p-p38/p38, p-p65/p65, NLRP3, and IL-1β, and up-regulated the levels of Bcl-2/Bax, p-Nrf2/Nrf2, and HO-1. The results suggested that CD could protect mice against LPS-induced acute lung injury by inhibiting oxidative stress, inflammation, and apoptosis via the TLR4-MAPKs/NF-κB signaling pathways.

Indexed as

Acute Lung InjuryNF-kappa BAnimalsApoptosisFlavonesInflammationLipopolysaccharidesMiceOxidative StressSignal TransductionToll-Like Receptor 4chrysosplenol DFlavonesLipopolysaccharidesNF-kappa BTlr4 protein, mouseToll-Like Receptor 4acute lung injuryapoptosischrysosplenol Dinflammationlipopolysaccharideoxidative stress

Identifiers

PMID34806444
PMCPMC8762090
OpenAlexW3214954317

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.