Evidence map›Paper›PMID 36617342›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2023

Inhibition of gp130 alleviates LPS-induced lung injury by attenuating apoptosis and inflammation through JAK1/STAT3 signaling pathway.

Fan Xu, Sijiao Wang, Yali Wang, Lijuan Hu, Lei Zhu

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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

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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

5 authors at 2 institutions in 1 country.

Fan XuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Feng Lin Road, Shanghai, 200032, People's Republic of China.
Sijiao WangDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Feng Lin Road, Shanghai, 200032, People's Republic of China.
Yali WangDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Feng Lin Road, Shanghai, 200032, People's Republic of China.
Lijuan HuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Feng Lin Road, Shanghai, 200032, People's Republic of China.
Lei ZhuDepartment of Pulmonary Medicine, Zhongshan Hospital, Fudan University, 180 Feng Lin Road, Shanghai, 200032, People's Republic of China. tfzhu@126.com.
Fudan University · CNZhongshan Hospital · CN

Funding

National Natural Science Foundation of China 81873420
6 · The paper itself

Abstract

BACKGROUND AND

objectiveAcute lung injury or acute respiratory distress syndrome (ALI/ARDS) is a life-threatening respiratory disease. Gp130 is a signal transduction receptor that participates in a variety of essential biological processes. The biological function of gp130 in ALI/ARDS is unclear. This study aims to investigate the roles and potential mechanisms of gp130 in lung injury induced by lipopolysaccharide (LPS).

methodsThe ALI/ARDS mouse model was established using intratracheal LPS administration. Hematoxylin and eosin staining and bronchoalveolar lavage fluid analysis were used to evaluate the degree of lung injury. Cell apoptosis was assessed by TUNEL staining, flow cytometry, and western blot. Then the expression of gp130, IL-6, IL-10, TNF-α, and the JAK1/STAT3 signaling pathway-related proteins was assessed by RT-PCR, western blot, and immunohistochemistry.

resultsThe expression of gp130 increased after 24 h of LPS treatment. Inhibiting gp130 improved inflammatory infiltration and alveolar collapsed, decreased IL-6 and TNF-α levels, raised IL-10 levels, and decreased cell apoptosis in LPS-induced mice. Meanwhile, suppressing gp130 reduced the inflammatory response and cell apoptosis in LPS-induced Beas-2B cells. Furthermore, p-JAK1 and p-STAT3 expressions were elevated after LPS stimulation and decreased following gp130 inhibition, suggesting that gp130 may regulate the JAK1/STAT3 signaling pathway in LPS-induced mice and Beas-2B cells.

conclusionThe findings suggest that gp130 regulates the inflammatory response and cell apoptosis through the JAK1/STAT3 signaling pathway, thereby mitigating LPS-induced lung injury. Gp130 may be a potential therapeutic target for ALI/ARDS.

Indexed as

Acute Lung InjuryRespiratory Distress SyndromeAnimalsApoptosisCytokine Receptor gp130InflammationInterleukin-10Interleukin-6LipopolysaccharidesLungMiceSignal TransductionTumor Necrosis Factor-alphaCytokine Receptor gp130Interleukin-10Interleukin-6LipopolysaccharidesTumor Necrosis Factor-alphaAcute lung injuryCell apoptosisgp130InflammationJAK1/STAT3

Identifiers

PMID36617342
OpenAlexW4313730610

What OpenQuestion holds

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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.