Evidence map›Paper›PMID 35889786›Full record

ArticleNutrients2022

Inosine Pretreatment Attenuates LPS-Induced Lung Injury through Regulating the TLR4/MyD88/NF-κB Signaling Pathway In Vivo.

Bingyong Mao, Weiling Guo, Xin Tang, Qiuxiang Zhang, Bo Yang, Jianxin Zhao, Shumao Cui, Hao Zhang

Open access · goldAbstract read
In one paragraph

Article in Nutrients, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  9. Review
  10. Review
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  13. Anti-Obesity Activity ofNutrients · 2024
    Article
  14. Optimized combination ofFood science and biotechnology · 2024
    Article
  15. Article
  16. Article
  17. Purinergic signaling pathway in severe COVID-19.Current opinion in pharmacology · 2023
    Review
  18. Article
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 at 1 institution in 1 country.

Bingyong MaoState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Weiling GuoState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Xin TangState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Qiuxiang ZhangState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.ORCID 0000-0003-2080-2214
Bo YangState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.ORCID 0000-0002-1347-3718
Jianxin ZhaoState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Shumao CuiState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Hao ZhangState Key Laboratory of Food Science and Technology, Jiangnan University, Wuxi 214122, China.
Jiangnan University · CN

Funding

National Natural Science Foundation of China 31972086National Natural Science Foundation of China 32072197National Natural Science Foundation of China 32172173
6 · The paper itself

Abstract

Inosine is a type of purine nucleoside, which is considered to a physiological energy source, and exerts a widely range of anti-inflammatory efficacy. The TLR4/MyD88/NF-κB signaling pathway is essential for preventing host oxidative stresses and inflammation, and represents a promising target for host-directed strategies to improve some forms of disease-related inflammation. In the present study, the results showed that inosine pre-intervention significantly suppressed the pulmonary elevation of pro-inflammatory cytokines (including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)), malondialdehyde (MDA), nitric oxide (NO), and reactive oxygen species (ROS) levels, and restored the pulmonary catalase (CAT), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and myeloperoxidase (MPO) activities (p < 0.05) in lipopolysaccharide (LPS)-treated mice. Simultaneously, inosine pre-intervention shifted the composition of the intestinal microbiota by decreasing the ratio of Firmicutes/Bacteroidetes, elevating the relative abundance of Tenericutes and Deferribacteres. Moreover, inosine pretreatment affected the TLR4/MyD88/NF-κB signaling pathway in the pulmonary inflammatory response, and then regulated the expression of pulmonary iNOS, COX2, Nrf2, HO-1, TNF-α, IL-1β, and IL-6 levels. These findings suggest that oral administration of inosine pretreatment attenuates LPS-induced pulmonary inflammatory response by regulating the TLR4/MyD88/NF-κB signaling pathway, and ameliorates intestinal microbiota disorder.

Indexed as

Acute Lung InjuryInosineNF-kappa BAnimalsInflammationLipopolysaccharidesMiceMyeloid Differentiation Factor 88Signal TransductionToll-Like Receptor 4Tumor Necrosis Factor-alphaInosineLipopolysaccharidesMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BTlr4 protein, mouseToll-Like Receptor 4Tumor Necrosis Factor-alphainosineintestinal microbiotalung injuryTLR4/MyD88/NF-κB

Identifiers

PMID35889786
PMCPMC9318366
OpenAlexW4285012275

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.