Evidence map›Paper›PMID 26231226›Full record

ArticleJournal of biomedical science2015

Osthole ameliorates hepatic fibrosis and inhibits hepatic stellate cell activation.

Ya-Wei Liu, Yung-Tsung Chiu, Shu-Ling Fu, Yi-Tsau Huang

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 50 citations in OpenAlex.

  1. Pooled it
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  15. [Endoplasmic reticulum stress enhances tumor necrosis factor-Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2020
    Article
  16. Phytochemistry, Ethnopharmacology, Pharmacokinetics and Toxicology ofInternational journal of molecular sciences · 2020
    Review
  17. Kupffer Cell-Derived TNF-BioMed research international · 2020
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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

4 authors at 3 institutions in 1 country.

Ya-Wei LiuInstitute of Traditional Medicine, School of Medicine, National Yang-Ming University, No. 155, Li-Nong Street, Sec. 2, Taipei, 11221, Taiwan. yaweiliu19850417@gmail.com.
Yung-Tsung ChiuDepartment of Medical Research and Education, Taichung Veterans General Hospital, No. 1650, Taiwan Boulevard Sec. 4, Taichung, 40705, Taiwan. ytchiu@vghtc.gov.tw.
Shu-Ling FuInstitute of Traditional Medicine, School of Medicine, National Yang-Ming University, No. 155, Li-Nong Street, Sec. 2, Taipei, 11221, Taiwan. slfu@ym.edu.tw.
Yi-Tsau HuangInstitute of Traditional Medicine, School of Medicine, National Yang-Ming University, No. 155, Li-Nong Street, Sec. 2, Taipei, 11221, Taiwan. huangyt@nricm.edu.tw.
National Yang Ming Chiao Tung University · TWNational Research Institute of Chinese Medicine · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHepatic fibrosis is a dynamic process which ultimately leads to cirrhosis in almost patients with chronic hepatic injury. However, progressive fibrosis is a reversible scarring response. Activation of hepatic stellate cells (HSCs) is the prevailing process during hepatic fibrosis. Osthole is an active component majorly contained in the fruit of Cnidium monnieri (L.) Cusson. This present study investigated the therapeutic effects of osthole on rat liver fibrosis and HSC activation.

resultsWe established the thioacetamide (TAA)-model of Sprague-Dawley (SD) rats to induce hepatic fibrosis. Rats were divided into three groups: control, TAA, and TAA + osthole (10 mg/kg). In vivo, osthole significantly reduced liver injury by diminishing levels of plasma AST and ALT, improving histological architecture, decreasing collagen and α-SMA accumulation, and improving hepatic fibrosis scores. Additionally, osthole reduced the expression of fibrosis-related genes significantly. Osthole also suppressed the production of fibrosis-related cytokines and chemokines. Moreover, nuclear translocation of p65 was significantly suppressed in osthole-treated liver. Osthole also ameliorated TAA-induced injury through reducing cellular oxidation. Osthole showed inhibitory effects in inflammation-related genes and chemokines production as well. In vitro, we assessed osthole effects in activated HSCs (HSC-T6 and LX-2). Osthole attenuated TGF-β1-induced migration and invasion in HSCs. Furthermore, osthole decreased TNF-α-triggered NF-κB activities significantly. Besides, osthole alleviated TGF-β1- or ET-1-induced HSCs contractility.

conclusionsOur study demonstrated that osthole improved TAA-caused liver injury, fibrogenesis and inflammation in rats. In addition, osthole suppressed HSCs activation in vitro significantly.

Indexed as

ActinsAnimalsCoumarinsCytokinesHepatic Stellate CellsLiver CirrhosisOxidation-ReductionRatsRats, Sprague-DawleyThioacetamideActinsCoumarinsCytokinesostholThioacetamide

Identifiers

PMID26231226
PMCPMC4522080
OpenAlexW2110309444

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.