Evidence map›Paper›PMID 26688180›Full record

ArticleChinese journal of integrative medicine2018

San-Cao Granule () Ameliorates Hepatic Fibrosis through High Mobility Group Box-1 Protein/Smad Signaling Pathway.

Shi-Zhang Wei, Sheng-Qiang Luo, Jian Wang, Jia-Bo Wang, Rui-Sheng Li, Xiao-Mei Zhang, Yan-Lei Guo, Chang Chen, Xiao Ma, Zhe Chen and 8 more

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Article in Chinese journal of integrative medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 30% 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

2 citing papers in PubMed, 5 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

18 authors at 4 institutions in 1 country.

Shi-Zhang WeiCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Sheng-Qiang LuoDepartment of Integrative Medical Center, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Jian WangCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Jia-Bo WangChina Military Institute of Chinese Medicine, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Rui-Sheng LiAnimal Laboratory Center, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Xiao-Mei ZhangCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Yan-Lei GuoChongqing Academy of Chinese Traditional Materia Medica, Key Laboratory of Chongqing Traditional Chinese Medicine Resources, Chongqing, 400065, China.
Chang ChenCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Xiao MaCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Zhe ChenCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Hong-Hong LiuDepartment of Integrative Medical Center, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Zhi-Rui YangCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Jian-Yu LiDepartment of Integrative Medical Center, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Rui-Lin WangDepartment of Integrative Medical Center, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Ya-Ming ZhangChina Military Institute of Chinese Medicine, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Hui-Yin YangDepartment of Integrative Medical Center, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Xiao-He XiaoChina Military Institute of Chinese Medicine, 302 Hospital of People's Liberation Army, Beijing, 100039, China.
Yan-Ling ZhaoCollege of Pharmacy, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China. zhaoyl22855@163.com.
302 Military Hospital of China · CNChinese People's Liberation Army · CNChengdu University of Traditional Chinese Medicine · CNChongqing Academy of Chinese Materia Medica · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo investigate the possible mechanism of San-Cao Granule (SCG, ) mediating antiliver fibrosis.

methodsA total of 60 male Sprague-Dawley rats were randomly divided into the normal control group, porcine serum-treated group, ursodesoxycholic acid (UDCA, 60 mg/kg), SCG (3.6 g/kg) group, SCG (1.8 g/kg) group and SCG (0.9 g/kg) group, with 10 rats in each group. Liver fibrosis was induced with porcine serum by intraperitoneal injection for 8 weeks, except for the normal control group. Then, the rats in the three SCG-treated groups and UDCA group were administered SCG and UDCA respectively for 4 weeks. The serum levels of alanine transaminase (ALT), aspartate transaminase (AST), albumin (ALB), total bilirubin (TBIL), hyaluronic acid (HA), laminin (LN), and type IV collagen (IVC) were examined using commercial kits and hepatic histopathology was examined with hematoxylin and eosin and Masson staining. Moreover, the protein expression levels of high mobility group box-1 protein (HMGB1), transforming growth factor β1 (TGF-β1), phosphorylated mothers against decapentaplegic homolog 3 (p-Smad3), Smad7, toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor-kappa B (NF-κB) and α-smooth muscle actin (α-SMA) were determined by western blot, immunohistochemistry and real time quantitative-reverse transcription polymerase.

resultsBoth SCG (3.6 and 1.8 g/kg) and UDCA significantly ameliorated the liver fibrosis induced by porcine serum as indicated by retarding the serum levels increasing of ALT, AST, TBIL, HA, LN and IVC and preventing the serum level reducing of ALB compared with the model group (all P<0.01). Meanwhile, the collagen deposition was attenuated by SCG and UDCA treatment. Furthermore, SCG markedly reduced the expressions of HMGB1, TGF-β1, p-Smad3, TLR4, MyD88, NF-κB and α-SMA, and enhanced the expression of the Smad7 compared with the model group (all P<0.01).

conclusionSCG ameliorates hepatic fibrosis possibly through inhibiting HMGB1, TLR4/NF-κB and TGF-β1/Smad signaling pathway.

Indexed as

AnimalsDisease Models, AnimalDrugs, Chinese HerbalHMGB1 ProteinLiverLiver CirrhosisMaleRatsRats, Sprague-DawleySignal TransductionSmad ProteinsDrugs, Chinese HerbalHMGB1 ProteinSan-Cao granulesSmad Proteinshigh mobility group box-1 proteinliver fibrosisSan-Cao Granuletoll-like receptor 4/nuclear factor-kappa Btransforming growth factor β1/mothers against decapentaplegic homolog

Identifiers

PMID26688180
OpenAlexW2287063556

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Registered trials

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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.