Evidence map›Paper›PMID 35287559›Full record

ArticleBioengineered2022

Protecting effect of emodin in experimental autoimmune encephalomyelitis mice by inhibiting microglia activation and inflammation via Myd88/PI3K/Akt/NF-κB signalling pathway.

Kenan Zheng, Baojiang Lv, Lulu Wu, Chen Wang, Haoyou Xu, Xiaojun Li, Zhibing Wu, Yuanqi Zhao, Zequan Zheng

Open access · goldAbstract read
In one paragraph

Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
12.6field-weighted citation impact, top 1% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 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

9 authors at 3 institutions in 1 country.

Kenan ZhengThe First Clinical School, Guangzhou University of Chinese Medicine, Guangzhou, China.
Baojiang LvThe First Clinical School, Guangzhou University of Chinese Medicine, Guangzhou, China.
Lulu WuThe First Clinical School, Guangzhou University of Chinese Medicine, Guangzhou, China.
Chen WangDepartment of Traditional Chinese Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
Haoyou XuDepartment of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, China.
Xiaojun LiThe Second Clinical School, Guangzhou University of Chinese Medicine, Guangzhou, China.
Zhibing WuDepartment of Neurology, The First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Yuanqi ZhaoDepartment of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, China.
Zequan ZhengDepartment of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Provincial Hospital of Traditional Chinese Medicine, Guangzhou, China.ORCID 0000-0002-4504-343X
Guangzhou University of Chinese Medicine · CNFirst Affiliated Hospital of Guangzhou University of Chinese Medicine · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is characterized by demyelination of the central nervous system. Emodin is an anthraquinone derivative with comprehensive anti-inflammatory, anti-cancer, and immunomodulatory effects and is widely used in the treatment of inflammatory, tumor, and immune system diseases. However, none of the clinical or experimental studies have explored the therapeutic efficacy of emodin in EAE/multiple sclerosis (MS). Thus, we evaluated the protective effect of emodin on EAE mediated via inhibition of microglia activation and inflammation. Wild-type mice were randomly divided into the normal control, EAE, low-dose emodin, and high-dose emodin groups. Clinical scores and pathological changes were assessed 21 days after immunization. The network pharmacology approach was used to elucidate the underlying mechanisms by using an online database. Molecular docking, polymerase-chain reaction tests, western blotting, and immunofluorescence were performed to verify the network pharmacology results. An

Indexed as

EmodinEncephalomyelitis, Autoimmune, ExperimentalAnimalsAnti-Inflammatory AgentsInflammationMiceMice, Inbred C57BLMicrogliaMolecular Docking SimulationMyeloid Differentiation Factor 88NF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSpinal CordAnti-Inflammatory AgentsEmodinMyd88 protein, mouseMyeloid Differentiation Factor 88NF-kappa BPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktemodinmicroglia activationMS/EAEmyelin protectivenetwork pharmacologyPI3K/AKT/NF- κB signalling pathwayTLRs/MyD88 signal

Identifiers

PMID35287559
PMCPMC9161934
OpenAlexW4220987261

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.