Evidence map›Paper›PMID 30809091›Full record

ArticleDrug design, development and therapy2019

Emodin induces apoptosis and autophagy of fibroblasts obtained from patient with ankylosing spondylitis.

Cong Ma, Bo Wen, Qin Zhang, Pei-Pei Shao, Wen Gu, Kun Qu, Yang Shi, Bei Wang

Open access · goldAbstract read
In one paragraph

Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

22 citing papers in PubMed, 41 citations in OpenAlex.

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  13. Mechanism of Emodin in the Treatment of Rheumatoid Arthritis.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

8 authors at 1 institution in 1 country.

Cong MaDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Bo WenDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Qin ZhangDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Pei-Pei ShaoDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Wen GuDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Kun QuDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Yang ShiDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Bei WangDepartment of Rheumatology and Immunology, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, People's Republic of China, macong_bhtcm@126.com.
Beijing Hospital of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAnkylosing spondylitis (AS) is a type of rheumatoid disease, which has been reported to be associated with the excessive proliferation of fibroblasts recently. Emodin, a single component from a traditional Chinese medicine

methodsFibroblasts obtained from patients with AS were used in the current study. In addition, multiple cellular and molecular biology techniques such as Cell Counting Kit-8, Western blotting, flow cytometry, monodansylcadaverine staining, and immunofluorescence assay were applied as well.

resultsEmodin-induced apoptosis of fibroblasts obtained from patient with AS via increasing active caspase-9, active caspase-3, and Bax levels and downregulating Bcl-2. Meanwhile, emodin enhanced autophagy in fibroblasts via upregulation of the expression of Atg12, Atg5, and Beclin 1, which was further confirmed by monodansylcadaverine staining. As expected, autophagy inhibitor 3-methyladenine (3MA) completely reversed emodin-induced autophagy in fibroblasts. Moreover, 3MA significantly increased emodin-induced apoptosis of fibroblasts obtained from patient with AS by increasing the levels of γH2AX, active caspase-9, active caspase-3, and cleaved poly ADP-ribose polymerase.

conclusionOur results indicated that emodin effectively induced apoptosis and autophagy of fibroblasts obtained from patient with AS. In addition, suppression of autophagy enhanced emodin-induced apoptosis in fibroblasts. Therefore, we proposed that combination of emodin with autophagy inhibitor might be a potent strategy for improving the symptoms of AS in the future.

Indexed as

AdultApoptosisAutophagyCell ProliferationDose-Response Relationship, DrugEmodinFemaleFibroblastsHumansMaleMiddle AgedMolecular StructureSpondylitis, AnkylosingStructure-Activity RelationshipEmodin3MAankylosing spondylitisapoptosisautophagyemodin

Identifiers

PMID30809091
PMCPMC6376879
OpenAlexW2912932892

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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.