Evidence map›Paper›PMID 33572510›Full record

ArticleAntioxidants (Basel, Switzerland)2021

Protective Effects of Kirenol against Lipopolysaccharide-Induced Acute Lung Injury through the Modulation of the Proinflammatory NFκB Pathway and the AMPK2-/Nrf2-Mediated HO-1/AOE Pathway.

Frank Cheau-Feng Lin, Shiuan-Shinn Lee, Yi-Ching Li, Yung-Chuan Ho, Wen-Ying Chen, Chun-Jung Chen, Min-Wei Lee, Kun-Lin Yeh, Stella Chin-Shaw Tsai, Yu-Hsiang Kuan

Open access · goldAbstract read
In one paragraph

Article in Antioxidants (Basel, Switzerland), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

12 citing papers in PubMed, 25 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

10 authors at 5 institutions in 1 country.

Frank Cheau-Feng LinSchool of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
Shiuan-Shinn LeeSchool of Public Health, Chung Shan Medical University, Taichung 40201, Taiwan.
Yi-Ching LiDepartment of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.
Yung-Chuan HoSchool of Medical Applied Chemistry, Chung Shan Medical University, Taichung 40201, Taiwan.
Wen-Ying ChenDepartment of Veterinary Medicine, National Chung Hsing University, Taichung 402204, Taiwan.ORCID 0000-0002-5105-5285
Chun-Jung ChenDepartment of Education and Research, Taichung Veterans General Hospital, Taichung 40705, Taiwan.
Min-Wei LeeA Graduate Institute of Microbiology and Public Health, National Chung Hsing University, Taichung 402204, Taiwan.
Kun-Lin YehDepartment of Veterinary Medicine, National Chung Hsing University, Taichung 402204, Taiwan.
Stella Chin-Shaw TsaiDa Vinci Surgical Center, Tungs' Taichung MetroHarbor Hospital, Taichung 435403, Taiwan.ORCID 0000-0003-2694-1207
Yu-Hsiang KuanDepartment of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung 40201, Taiwan.ORCID 0000-0002-8991-6394
Chung Shan Medical University Hospital · TWNational Chung Hsing University · TWChung Shan Medical University · TWTaichung Veterans General Hospital · TWTungs' Taichung MetroHarbor Hospital · TW

Funding

Ministry of Science and Technology, Taiwan 109-2635-B-860-001-
6 · The paper itself

Abstract

Acute lung injury (ALI) is an acute and life-threatening inflammatory disease of the lung parenchyma that is associated with high mortality worldwide. No therapeutic strategies have been developed for the mitigation of the proinflammatory response that characterizes ALI. Kirenol has anti-inflammatory, antiarthritic, and immunoregulatory effects. In the present study, we investigated the protective effects of kirenol against lipopolysaccharides (LPS)-induced ALI in mice. Kirenol reduced the LPS-induced histopathology changes involving edema and thickening of the interstitial or alveolar walls, infiltration of leukocytes, formation of hyaline membrane. Pretreatment with kirenol reduced leukocytes infiltration in bronchoalveolar lavage fluid (BALF), the alveolar-capillary barrier disruption and lipid peroxidation in lung tissues induced by LPS. Kirenol significantly inhibited the secretion of cytokines, IL-1β, IL6, and TNFα, into the BALF of the mice with LPS-induced ALI through NFκB activation. Moreover, kirenol attenuated the downregulation of the antioxidant enzymes, superoxide dismutase, glutathione peroxidase, and catalase that was induced by LPS. HO-1 expression and the phosphorylation of Nrf2 and AMPK2 were also induced by kirenol. The results indicate that kirenol can be developed as a treatment strategy for ALI, and its effects are induced through the inhibition of the NF-κB proinflammatory pathway and promotion of AMPK2/Nrf2-mediated HO-1 and antioxidant enzymes (AOE) activation.

Indexed as

acute lung injuryAMPK2/Nrf2-mediated HO-1AOE pathwaykirenollipopolysaccharideNF-κB pathway

Identifiers

PMID33572510
PMCPMC7911485
OpenAlexW3126876954

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.