Evidence map›Paper›PMID 34863181›Full record

ArticleRespiratory research2021

Ferulic acid ameliorates lipopolysaccharide-induced tracheal injury via cGMP/PKGII signaling pathway.

Xiaoyong Xie, Tong Yu, Yapeng Hou, Aixin Han, Yan Ding, Hongguang Nie, Yong Cui

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 40% 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

6 citing papers in PubMed, 7 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

7 authors at 2 institutions in 1 country.

Xiaoyong Xie *Department of Anesthesiology, the First Hospital of China Medical University, Shenyang, 110001, China.
Tong Yu *Department of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, 110122, China.
Yapeng HouDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, 110122, China.
Aixin HanDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, 110122, China.
Yan DingDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, 110122, China.
Hongguang NieDepartment of Stem Cells and Regenerative Medicine, College of Basic Medical Science, China Medical University, Shenyang, 110122, China. hgnie@cmu.edu.cn.
Yong CuiDepartment of Anesthesiology, the First Hospital of China Medical University, Shenyang, 110001, China. ycui@cmu.edu.cn.ORCID http://orcid.org/0000-0002-8613-010X
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

National Natural Science Foundation of China 81670010National Natural Science Foundation of China 82170093
6 · The paper itself

Abstract

backgroundTracheal injury is a common clinical condition that still lacks an effective therapy at present. Stimulation of epithelial sodium channel (ENaC) increases Na

methodsC57BL/J male mice were treated intraperitoneally with normal saline or FA (100 mg/kg) 12 h before, and 12 h after intratracheal administration of lipopolysaccharide (LPS, 5 mg/kg), respectively. The effects of FA on tracheal injury were not only assessed through HE staining, immunofluorescence assay, and protein/mRNA expressions of ENaC located on tracheas, but also evaluated by the function of ENaC in mouse tracheal epithelial cells (MTECs). Besides, to explore the detailed mechanism about FA involved in LPS-induced tracheal injury, the content of cyclic guanosine monophosphate (cGMP) was measured, and Rp-cGMP (cGMP inhibitor) or cGMP-dependent protein kinase II (PKGII)-siRNA (siPKGII) were applied in primary MTECs, respectively.

resultsHistological examination results demonstrated that tracheal injury was obviously attenuated by pretreatment of FA. Meanwhile, FA could reverse LPS-induced reduction of both protein/mRNA expressions and ENaC activity. ELISA assay verified cGMP content was increased by FA, and administration of Rp-cGMP or transfection of siPKGII could reverse the FA up-regulated ENaC protein expression in MTECs.

conclusionsFerulic acid can attenuate LPS-induced tracheal injury through up-regulation of ENaC at least partially via the cGMP/PKGII pathway, which may provide a promising new direction for preventive and therapeutic strategy in tracheal injury.

Indexed as

Gene Expression RegulationAcute Lung InjuryAnimalsCells, CulturedCoumaric AcidsCyclic GMP-Dependent Protein Kinase Type IIEnzyme-Linked Immunosorbent AssayEpithelial Sodium ChannelsFree Radical ScavengersLipopolysaccharidesMaleMiceMice, Inbred C57BLRNASignal TransductionTracheaCoumaric AcidsCyclic GMP-Dependent Protein Kinase Type IIEpithelial Sodium Channelsferulic acidFree Radical ScavengersLipopolysaccharidesRNAcGMP/PKGII signaling pathwayEpithelial sodium channelFerulic acidTracheal injury

Identifiers

PMID34863181
PMCPMC8642995
OpenAlexW4200526009

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Registered trials

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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.