Evidence map›Paper›PMID 35453467›Full record

ArticleAntioxidants (Basel, Switzerland)2022

HO-1 Upregulation by Kaempferol via ROS-Dependent Nrf2-ARE Cascade Attenuates Lipopolysaccharide-Mediated Intercellular Cell Adhesion Molecule-1 Expression in Human Pulmonary Alveolar Epithelial Cells.

Chien-Chung Yang, Li-Der Hsiao, Chen-Yu Wang, Wei-Ning Lin, Ya-Fang Shih, Yi-Wen Chen, Rou-Ling Cho, Hui-Ching Tseng, Chuen-Mao Yang

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 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
2.3field-weighted citation impact, top 11% 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.

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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

9 authors at 3 institutions in 1 country.

Chien-Chung YangDepartment of Traditional Chinese Medicine, Chang Gung Memorial Hospital at Tao-Yuan, Kwei-San, Tao-Yuan 33302, Taiwan.ORCID 0000-0003-2325-5017
Li-Der HsiaoDepartment of Pharmacology, College of Medicine, China Medical University, Taichung 40402, Taiwan.
Chen-Yu WangDepartment of Pharmacology, College of Medicine, China Medical University, Taichung 40402, Taiwan.
Wei-Ning LinGraduate Institute of Biomedical and Pharmaceutical Science, Fu Jen Catholic University, New Taipei City 242, Taiwan.ORCID 0000-0003-3205-871X
Ya-Fang ShihDepartment of Pharmacology, College of Medicine, China Medical University, Taichung 40402, Taiwan.
Yi-Wen ChenDepartment of Pharmacology, College of Medicine, China Medical University, Taichung 40402, Taiwan.
Rou-Ling ChoDepartment of Pharmacology, College of Medicine, China Medical University, Taichung 40402, Taiwan.ORCID 0000-0002-8970-5562
Hui-Ching TsengDepartment of Pharmacology, College of Medicine, China Medical University, Taichung 40402, Taiwan.
Chuen-Mao YangDepartment of Pharmacology, College of Medicine, China Medical University, Taichung 40402, Taiwan.ORCID 0000-0002-3208-5438
Asia University · TWChina Medical University · TWFu Jen Catholic University · TW

Funding

Chang Gung Medical Research Foundation, Taiwan CMRPG5J0142Chang Gung Medical Research Foundation, Taiwan CMRPG5J0143Chang Gung Medical Research Foundation, Taiwan CMRPG5L0181China Medical University, Taiwan CMU110-MF-05Ministry of Science and Technology, Taiwan MOST109-2320-B-039-061Ministry of Science and Technology, Taiwan MOST110-2320-B-039-071
6 · The paper itself

Abstract

Lung inflammation is a pivotal event in the pathogenesis of acute lung injury. Heme oxygenase-1 (HO-1) is a key antioxidant enzyme that could be induced by kaempferol (KPR) and exerts anti-inflammatory effects. However, the molecular mechanisms of KPR-mediated HO-1 expression and its effects on inflammatory responses remain unknown in human pulmonary alveolar epithelial cells (HPAEpiCs). This study aimed to verify the relationship between HO-1 expression and KPR treatment in both in vitro and in vivo models. HO-1 expression was determined by real time-PCR, Western blotting, and promoter reporter analyses. The signaling components were investigated by using pharmacological inhibitors or specific siRNAs. Chromatin immunoprecipitation (ChIP) assay was performed to investigate the interaction between nuclear factor erythroid-2-related factor (Nrf2) and antioxidant response elements (ARE) binding site of HO-1 promoter. The effect of KPR on monocytes (THP-1) binding to HPAEpiCs challenged with lipopolysaccharides (LPS) was determined by adhesion assay. We found that KPR-induced HO-1 level attenuated the LPS-induced intercellular cell adhesion protein 1 (ICAM-1) expression in HPAEpiCs. KPR-induced HO-1 mRNA and protein expression also attenuated ICAM-1 expression in mice. Tin protoporphyrin (SnPP)IX reversed the inhibitory effects of KPR in HPAEpiCs. In addition, in HPAEpiCs, KPR-induced HO-1 expression was abolished by both pretreating with the inhibitor of NADPH oxidase (NOX, apocynin (APO)), reactive oxygen species (ROS) (N-acetyl-L-cysteine (NAC)), Src (Src kinase inhibitor II (Srci II)), Pyk2 (PF431396), protein kinase C (PKC)α (Gö6976), p38 mitogen-activated protein kinase (MAPK) inhibitor (p38i) VIII, or c-Jun N-terminal kinases (JNK)1/2 (SP600125) and transfection with their respective siRNAs. The transcription of the

Indexed as

HO-1human pulmonary alveolar epithelial cellsinflammationkaempferolLPS

Identifiers

PMID35453467
PMCPMC9028455
OpenAlexW4224142224

What Socratic 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 Socratic graph.