Evidence map›Paper›PMID 31827712›Full record

ArticleOxidative medicine and cellular longevity2019

Nerolidol Suppresses the Inflammatory Response during Lipopolysaccharide-Induced Acute Lung Injury via the Modulation of Antioxidant Enzymes and the AMPK/Nrf-2/HO-1 Pathway.

Yung-Lun Ni, Huan-Ting Shen, Chun-Hung Su, Wen-Ying Chen, Rosa Huang-Liu, Chun-Jung Chen, Shih-Pin Chen, Yu-Hsiang Kuan

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
2.4field-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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.

  1. Pooled it
  2. Article
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  12. Targeting AMP-activated protein kinase in sepsis.Frontiers in endocrinology · 2024
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  17. Mechanism ofCancers · 2023
    Article
  18. Review
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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

8 authors at 5 institutions in 1 country.

Yung-Lun NiDepartment of Pulmonary Medicine, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan.
Huan-Ting ShenDepartment of Pulmonary Medicine, Taichung Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Taichung, Taiwan.
Chun-Hung SuDepartment of Internal Medicine, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Wen-Ying ChenDepartment of Veterinary Medicine, National Chung Hsing University, Taichung, Taiwan.
Rosa Huang-LiuSchool of Nutrition, Chung Shan Medical University, Taichung, Taiwan.
Chun-Jung ChenDepartment of Education and Research, Taichung Veterans General Hospital, Taichung, Taiwan.
Shih-Pin Chen *Department of Internal Medicine, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.
Yu-Hsiang Kuan *Department of Pharmacology, School of Medicine, Chung Shan Medical University, Taichung, Taiwan.ORCID https://orcid.org/0000-0002-8991-6394
Chung Shan Medical University Hospital · TWTaipei Tzu Chi Hospital · TWChung Shan Medical University · TWNational Chung Hsing University · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute lung injury (ALI) is a life-threatening disease that is characterised by the rapid onset of inflammatory responses. Lipopolysaccharide (LPS) is an endotoxin that plays an important role in triggering ALI via pneumonia and sepsis. However, no effective therapeutic strategies are currently available to treat ALI. Nerolidol is an aliphatic sesquiterpene alcohol that is found in the essential oils of many flowers as well as floral plants. It has been shown to exhibit anti-inflammatory, antioxidant, and anticancer properties. Herein, we show that nerolidol pretreatment counteracted the histopathological hallmarks in LPS-induced ALI mice. Indeed, nerolidol pretreatment inhibited LPS-induced alveolar-capillary barrier disruption, lung edema, and lipid peroxidation. Moreover, nerolidol pretreatment prevented the LPS from decreasing the enzymatic activities of superoxide dismutase, catalase, and glutathione peroxidase. Importantly, nerolidol treatment enhanced phosphorylation of AMP-activated protein kinase (AMPK) and expression of nuclear factor erythroid-derived 2-related factor 2 (Nrf-2) and heme oxygenase-1 (HO-1). Taken together, our study reveals the novel protective effects of nerolidol in LPS-induced ALI via the induction of antioxidant responses and activation of the AMPK/Nrf-2/HO-1 signalling pathway.

Indexed as

Acute Lung InjuryAMP-Activated Protein KinasesAnimalsAnti-Inflammatory AgentsAntioxidantsGene Expression RegulationHeme Oxygenase (Decyclizing)LipopolysaccharidesMaleMiceMice, Inbred BALB CNF-E2-Related Factor 2Oxidative StressPneumoniaSesquiterpenesSignal TransductionAMP-Activated Protein KinasesAnti-Inflammatory AgentsAntioxidantsHeme Oxygenase (Decyclizing)Hmox1 protein, ratLipopolysaccharidesnerolidolNfe2l2 protein, ratNF-E2-Related Factor 2Sesquiterpenes

Identifiers

PMID31827712
PMCPMC6885193
OpenAlexW2987333184

What OpenQuestion holds

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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.