Evidence map›Paper›PMID 25926716›Full record

ArticleDrug design, development and therapy2015

Schisandrin B inhibits cell growth and induces cellular apoptosis and autophagy in mouse hepatocytes and macrophages: implications for its hepatotoxicity.

Yi Zhang, Zhi-Wei Zhou, Hua Jin, Chengbin Hu, Zhi-Xu He, Zhi-Ling Yu, Kam-Ming Ko, Tianxin Yang, Xueji Zhang, Si-Yuan Pan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 24 citations in OpenAlex.

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  14. Lysine-Specific Demethylase 1 (LSD1) Inhibitor S2101 Induces Autophagy via the AKT/mTOR Pathway in SKOV3 Ovarian Cancer Cells.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Article
  15. Magnolol pretreatment attenuates heat stress-induced IEC-6 cell injury.Journal of Zhejiang University. Science. B · 2016
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  16. 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

11 authors at 7 institutions in 3 countries.

Yi ZhangDepartment of Pharmacology, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, People's Republic of China ; Department of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA.
Zhi-Wei ZhouDepartment of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA.
Hua JinDepartment of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA.
Chengbin HuDepartment of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA.
Zhi-Xu HeGuizhou Provincial Key Laboratory for Regenerative Medicine, Stem Cell and Tissue Engineering Research Center and Sino-US Joint Laboratory for Medical Sciences, Guiyang Medical University, Guiyang, Guizhou, People's Republic of China.
Zhi-Ling YuSchool of Chinese Medicine, Hong Kong Baptist University, Hong Kong, People's Republic of China.
Kam-Ming KoDivision of Life Science, Hong Kong University of Science and Technology, Hong Kong, People's Republic of China.
Tianxin YangDepartment of Internal Medicine, University of Utah and Salt Lake Veterans Affairs Medical Center, Salt Lake City, UT, USA.
Xueji ZhangResearch Center for Bioengineering and Sensing Technology, University of Science and Technology Beijing, Beijing, People's Republic of China.
Si-Yuan PanDepartment of Pharmacology, School of Chinese Materia Medica, Beijing University of Chinese Medicine, Beijing, People's Republic of China.
Shu-Feng ZhouDepartment of Pharmaceutical Sciences, College of Pharmacy, University of South Florida, Tampa, FL, USA.
University of South Florida · USBeijing University of Chinese Medicine · CNGuiyang Medical University · CNHong Kong Baptist University · HKHong Kong University of Science and Technology · HKUniversity of Science and Technology Beijing · CNUniversity of Utah · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A number of drugs and herbal compounds have been documented to cause hepatoxicity. Schisandrin B (Sch B) is an active dibenzocyclooctadiene isolated from Schisandrae fructus, with a wide array of pharmacological activities. However, the potential hepatotoxicity of Sch B is a major safety concern, and the underlying mechanism for Sch B-induced liver toxic effects is not fully elucidated. In the present study, we aimed to investigate the liver toxic effects and the molecular mechanisms of Sch B in mouse liver and macrophage cells. The results have shown that Sch B exhibits potent grow inhibitory, proapoptotic, and proautophagic effects in AML-12 and RAW 264.7 cells. Sch B markedly arrested cells in G1 phase in both cell lines, accompanied by the down-regulation of cyclin dependent kinase 2 (CDK2) and cyclin D1 and up-regulation of p27 Kip1 and checkpoint kinase 1. Furthermore, Sch B markedly increased the apoptosis of AML-12 and RAW 264.7 cells with a decrease in the expression of B-cell lymphoma-extra-large and (Bcl-xl) B-cell lymphoma 2 (Bcl-2), but an increase in the expression of B-cell lymphoma 2-associated X protein (Bax). Sch B promoted the cleavage of caspase 3 and poly-adenosine diphosphate-ribose polymerase (PARP) in both cell lines. Additionally, Sch B significantly induced autophagy of AML-12 and RAW 264.7 cells. Sch B inhibited the activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway, as indicated by their altered phosphorylation, contributing to the proautophagic effect of Sch B. Taken together, our findings show that the inducing effects of Sch B on cell cycle arrest, apoptosis, and autophagy may contribute to its liver toxic effects, which might provide a clue for the investigation of the molecular toxic targets and underlying mechanisms for Sch B-induced hepatotoxicity in herbal consumers. More studies are warranted to fully delineate the underlying mechanisms, efficacy, and safety of Sch B for clinical use.

Indexed as

AnimalsApoptosisAutophagyCell CycleCell DivisionCell LineCell SurvivalChemical and Drug Induced Liver InjuryCyclooctanesG1 PhaseHepatocytesLignansMacrophagesMiceMitochondria, LiverPolycyclic CompoundsCyclooctanesLignansPolycyclic Compoundsschizandrin BAML-12 cellBcl-2herbal medicineliver toxicitymTORRAW 264.7 cell

Identifiers

PMID25926716
PMCPMC4403607
OpenAlexW2034488296

What OpenQuestion holds

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LicenceCC BY-NC
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.