Evidence map›Paper›PMID 22363627›Full record

ArticlePloS one2012

Asiatic acid inhibits liver fibrosis by blocking TGF-beta/Smad signaling in vivo and in vitro.

Li-xia Tang, Rui-hua He, Guang Yang, Jia-ju Tan, Li Zhou, Xiao-ming Meng, Xiao Ru Huang, Hui Yao Lan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

47 citing papers in PubMed, 125 citations in OpenAlex.

  1. Review
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  12. Taxifolin, Extracted from WasteDrug design, development and therapy · 2021
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  15. International journal of molecular sciences · 2019
    Article
  16. Article
  17. A Compound of Chinese Herbs Protects against Alcoholic Liver Fibrosis in Rats via the TGF-Evidence-based complementary and alternative medicine : eCAM · 2019
    Article
  18. Article
  19. Article
  20. Asiatic acid ameliorates CClDrug design, development and therapy · 2018
    Article
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 3 institutions in 1 country.

Li-xia TangInstitute of Medical Research, The First People's Hospital of Foshan, Foshan, Guangdong, China.
Rui-hua He
Guang Yang
Jia-ju Tan
Li Zhou
Xiao-ming Meng
Xiao Ru Huang
Hui Yao Lan
First People's Hospital of Foshan · CNChinese University of Hong Kong · CNWest China Hospital of Sichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver fibrosis is a major cause of liver failure, but treatment remains ineffective. In the present study, we investigated the mechanisms and anti-hepatofibrotic activities of asiatic acid (AA) in a rat model of liver fibrosis induced by carbon tetrachloride (CCl(4)) and in vitro in TGF-beta1-stimulated rat hepatic stellate cell line (HSC-T6). Treatment with AA significantly attenuated CCl(4)-induced liver fibrosis and functional impairment in a dosage-dependent manner, including blockade of the activation of HSC as determined by inhibiting de novo alpha smooth muscle actin (a-SMA) and collagen matrix expression, and an increase in ALT and AST (all p<0.01). The hepatoprotective effects of AA on fibrosis were associated with upregulation of hepatic Smad7, an inhibitor of TGF-beta signaling, thereby blocking upregulation of TGF-beta1 and CTGF and the activation of TGF-beta/Smad signaling. The anti-fibrosis activity and mechanisms of AA were further detected in vitro in HSC-T6. Addition of AA significantly induced Smad7 expression by HSC-T6 cells, thereby inhibiting TGF-beta1-induced Smad2/3 activation, myofibroblast transformation, and collagen matrix expression in a dosage-dependent manner. In contrast, knockdown of Smad7 in HSC-T6 cells prevented AA-induced inhibition of HSC-T6 cell activation and fibrosis in response to TGF-beta1, revealing an essential role for Smad7 in AA-induced anti-fibrotic activities during liver fibrosis in vivo and in vitro. In conclusion, AA may be a novel therapeutic agent for liver fibrosis. Induction of Smad7-dependent inhibition of TGF-beta/Smad-mediated fibrogenesis may be a central mechanism by which AA protects liver from injury.

Indexed as

AnimalsBlotting, WesternCarbon TetrachlorideCell LineCollagen Type IGene Knockdown TechniquesHepatic Stellate CellsImmunohistochemistryLiverLiver CirrhosisLiver Function TestsMalePentacyclic TriterpenesPhosphorylationRatsRats, Sprague-Dawleyasiatic acidCarbon TetrachlorideCollagen Type IPentacyclic TriterpenesSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID22363627
PMCPMC3280334
OpenAlexW2029875051

What OpenQuestion holds

Textmetadata
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.