Evidence map›Paper›PMID 29970958›Full record

ArticleDrug design, development and therapy2018

Salidroside ameliorates autophagy and activation of hepatic stellate cells in mice via NF-κB and TGF-β1/Smad3 pathways.

Jiao Feng, Kan Chen, Yujing Xia, Liwei Wu, Jingjing Li, Sainan Li, Wenwen Wang, Xiya Lu, Tong Liu, Chuanyong Guo

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

32 citing papers in PubMed, 69 citations in OpenAlex.

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  14. Therapeutic effects of salidroside vs pyrrolidine dithiocarbamate against severe acute pancreatitis in rat.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022
    Article
  15. Pathogenesis of Liver Fibrosis and Its TCM Therapeutic Perspectives.Evidence-based complementary and alternative medicine : eCAM · 2022
    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

10 authors at 2 institutions in 1 country.

Jiao FengDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Kan ChenDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Yujing XiaDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Liwei WuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Jingjing LiDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Sainan LiDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Wenwen WangDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Xiya LuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Tong LiuDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Chuanyong GuoDepartment of Gastroenterology, Shanghai Tenth People's Hospital, Tongji University School of Medicine, Shanghai, China.
Shanghai Tenth People's Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeLiver fibrosis is commonly seen and a necessary stage in chronic liver disease. The aim of this study was to explore the effect of salidroside on liver fibrosis in mice and its potential mechanisms. MATERIALS AND

methodsTwo mouse liver fibrosis models were established by intraperitoneal injection of carbon tetrachloride (CCl

resultsSalidroside inhibited the production of extracellular matrix (ECM) and regulated the balance between MMP2 and TIMP1 and, therefore, alleviated liver fibrosis in the two fibrosis models. Salidroside reduced the production of transforming growth factor (TGF)-β1 in Kupffer cells and hepatic stellate cells (HSCs) via the nuclear factor-κB signaling pathway and, therefore, inhibited the activation of HSCs and autophagy by downregulation of the TGF-β1/Smad3 signaling pathway.

conclusionSalidroside can effectively attenuate liver fibrosis by inhibiting the activation of HSCs in mice.

Indexed as

AnimalsAutophagyGlucosidesHepatic Stellate CellsLiver CirrhosisMaleMiceMice, Inbred C57BLNF-kappa BPhenolsSignal TransductionSmad3 ProteinTransforming Growth Factor beta1GlucosidesNF-kappa BPhenolsrhodiolosideSmad3 ProteinSmad3 protein, mouseTransforming Growth Factor beta1autophagyhepatic stellate cellsliver fibrosissalidrosideTGF-β1/Smad3

Identifiers

PMID29970958
PMCPMC6021006
OpenAlexW2809139588

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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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.