Evidence map›Paper›PMID 31907823›Full record

ArticleSleep & breathing = Schlaf & Atmung2020

Astragaloside IV ameliorates intermittent hypoxia-induced inflammatory dysfunction by suppressing MAPK/NF-κB signalling pathways in Beas-2B cells.

Jian-Kun Chen, Ming-Kai Guo, Xiao-Hui Bai, Li-Qin Chen, Shun-Mei Su, Li Li, Ji-Qiang Li

Abstract read
PubMed Publisher
In one paragraph

Article in Sleep & breathing = Schlaf & Atmung, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.5field-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

17 citing papers in PubMed, 28 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 1 institution in 1 country.

Jian-Kun ChenThe Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Ming-Kai GuoThe Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Xiao-Hui BaiThe Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Li-Qin ChenThe Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Shun-Mei SuThe Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510120, China.
Li LiThe First Respiratory Department, The First People's Hospital of Kashi, Xinjiang, 844000, China. lili5511128@sina.com.
Ji-Qiang LiThe Second Clinical College, Guangzhou University of Chinese Medicine, Guangzhou, 510120, China. lijiqiangjizhen@163.com.
Guangzhou University of Chinese Medicine · CN

Funding

Guangdong Provincial Bureau of Chinese Medicine 20173023Guangdong Provincial Bureau of Chinese Medicine 20191158Guangdong Provincial Hospital of Chinese Medicine YN2019ML11Guangdong Provincial Hospital of Chinese Medicine YN2019QJ13
6 · The paper itself

Abstract

purposeIntermittent hypoxia is a characteristic pathological change in obstructive sleep apnoea (OSA) that can initiate oxidative stress reaction and pro-inflammatory cytokine release. The purpose of this study was to assess the effect and protective mechanism of Astragaloside IV (AS-IV) in intermittent hypoxia-induced human lung epithelial Beas-2B cells.

methodsHuman lung epithelial Beas-2B cells were exposed to intermittent hypoxia or normoxia in the absence or presence of AS-IV. MTT assay was performed to determine the cell viability. The levels of reactive oxygen species (ROS), lactate dehydrogenase (LDH), malonaldehyde (MDA), and superoxide dismutase (SOD) were measured to evaluate oxidative stress. The levels of cytokines interleukin (IL)-8, IL-1β, and IL-6 were evaluated by enzyme-linked immunosorbent assay and real-time PCR. The expression of Toll-like receptor 4 (TLR4), mitogen-activated protein kinase (MAPK), and nuclear transcription factor-kappa B (NF-κB) signalling pathways was analysed by western blot.

resultsThe results showed that AS-IV significantly reduced the levels of ROS, LDH, MDA, IL-8, IL-1β, and IL-6, and increased the level of SOD in intermittent hypoxia-induced Beas-2B cells. It also suppressed the phosphorylation of MAPKs, including P38, c-Jun N-terminal kinase and extracellular signal-regulated kinase, and inhibited the activation of the NF-κB signalling pathway by reducing the phosphorylation of IκBα and p65.

conclusionsAS-IV attenuates inflammation and oxidative stress by inhibiting TLR4-mediated MAPK/NF-κB signalling pathways in intermittent hypoxia-induced Beas-2B cells.

Indexed as

Cells, CulturedHumansHypoxiaInflammationLungMAP Kinase Signaling SystemNF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesRespiratory MucosaSaponinsSleep Apnea, ObstructiveTriterpenesastragaloside ANF-kappaB-Inducing KinaseProtein Serine-Threonine KinasesSaponinsTriterpenesAstragaloside IVIntermittent hypoxiaNF-κBObstructive sleep apnoea

Identifiers

PMID31907823
OpenAlexW2998459606

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.