Evidence map›Paper›PMID 34160729›Full record

ArticleInflammation2021

Glutamine Supplementation Attenuates the Inflammation Caused by LPS-Induced Acute Lung Injury in Mice by Regulating the TLR4/MAPK Signaling Pathway.

Jie Huang, Jing Liu, Guangjun Chang, Yan Wang, Nana Ma, Animesh Chadra Roy, Xiangzhen Shen

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2021. 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
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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  10. Food Peptides for the Nutricosmetic Industry.Antioxidants (Basel, Switzerland) · 2023
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. [Gambogic acid protects against lipopolysaccharide-induced acute lung injury via the MAPK signaling pathway].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics
    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

7 authors at 1 institution in 1 country.

Jie HuangCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
Jing LiuCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
Guangjun ChangCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
Yan WangCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
Nana MaCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
Animesh Chadra RoyCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China.
Xiangzhen ShenCollege of Veterinary Medicine, Nanjing Agricultural University, Nanjing, 210095, Jiangsu Province, China. xzshen@njau.edu.cn.ORCID http://orcid.org/0000-0002-0105-0670
Nanjing Agricultural University · CN

Funding

the National Key R&D Program of China 2017YFD0502205the Priority Academic Program Development of Jiangsu Higher Education Institutions PAPD
6 · The paper itself

Abstract

Bacterial infection is one of the main causes of bovine respiratory disease (BRD), which can cause tremendous losses for the herd farming industry worldwide. L-Glutamine (GLN), a neutral amino acid, has been reported to have anti-inflammatory properties. This study aims to explore the potential protective effects and mechanisms of GLN on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in mice. Forty ICR mice were randomly divided into four groups (n = 10): a PBS intratracheal instillation group, a LPS intratracheal instillation group, a GLN gavage group, and a LPS+GLN group (GLN was given 1 h before the LPS stimulation). Twelve hours after LPS administration, the lung tissue and blood were collected. The results showed that the concentrations of IL-6, IL-8, and IL-1β; the protein abundance of the toll-like receptor 4 (TLR4), phosphorylated p38 (p-p38), phosphorylated ERK1/2 (p-ERK1/2), and phosphorylated JNK (p-JNK); and the expression level of genes associated with inflammation, such as IL-1β, IL-8, TNF-α, IL-6, TLR4, p38, ERK1/2, and JNK, were significantly increased in the LPS group compared with those in the PBS group. However, these increases were attenuated by GLN pretreatment in the LPS+GLN group. Furthermore, the pathological change of the structure of lung tissue from the LPS group was obvious compared to that from the PBS group; however, with GLN administration, these pathological changes were alleviated. Additionally, the secretion level of mucus and the percentage of positive MUC5AC staining on the epithelial surface area of the airway increased dramatically in the LPS group; however, GLN pretreatment in the LPS+GLN group markedly decreased these phenomena compared with that of the LPS group. These results indicate that GLN supplementation ameliorates LPS-induced ALI in mice and this effect may be mediated by the TLR4/MAPK signaling pathway.

Indexed as

Acute Lung InjuryAnimalsAnti-Inflammatory AgentsCytokinesDisease Models, AnimalFemaleGlutamineInflammation MediatorsLipopolysaccharidesLungMiceMice, Inbred ICRMitogen-Activated Protein KinasesPhosphorylationPneumoniaSignal TransductionAnti-Inflammatory AgentsCytokinesGlutamineInflammation MediatorsLipopolysaccharidesMitogen-Activated Protein KinasesTlr4 protein, mouseToll-Like Receptor 4acute lung injury (ALI)glutamineinflammationlipopolysaccharide (LPS)

Identifiers

PMID34160729
OpenAlexW3175221832

What OpenQuestion holds

Textmetadata
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.