Evidence map›Paper›PMID 32581820›Full record

ArticleFrontiers in pharmacology2020

Icariin Attenuates Amyloid-β (Aβ)-Induced Neuronal Insulin Resistance Through PTEN Downregulation.

Xiaomei Zou, Xiyao Feng, Yalin Fu, Yuyang Zheng, Mingke Ma, Changhua Wang, Yemin Zhang

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
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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

7 authors at 4 institutions in 1 country.

Xiaomei ZouNeurology Center, The Second People's Hospital of Jingzhou City, Jingzhou, China.
Xiyao Feng2018 Clinical Medicine, Hubei University of Medicine, Shiyan, China.
Yalin FuDepartment of Pathology & Pathophysiology, Wuhan University School of Basic Medical Sciences, Wuhan, China.
Yuyang ZhengDepartment of Pathology & Pathophysiology, Wuhan University School of Basic Medical Sciences, Wuhan, China.
Mingke MaDepartment of Pathology & Pathophysiology, Wuhan University School of Basic Medical Sciences, Wuhan, China.
Changhua WangDepartment of Pathology & Pathophysiology, Wuhan University School of Basic Medical Sciences, Wuhan, China.
Yemin ZhangDepartment of Pathology & Pathophysiology, Wuhan University School of Basic Medical Sciences, Wuhan, China.
Hubei Provincial Center for Disease Control and Prevention · CNHubei University of Medicine · CNWuhan University · CNXian Yang Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuronal insulin resistance is implicated in neurodegenerative diseases. Icariin has been reported to improve insulin resistance in skeletal muscle cells and to restore impaired hypothalamic insulin signaling in the rats with chronic unpredictable mild stress. In addition, icariin can exert the neuroprotective effects in the mouse models of neurodegenerative diseases. However, the molecular mechanisms by which icariin affects neuronal insulin resistance are poorly understood. In the present study, amyloid-β (Aβ) was used to induce insulin resistance in human neuroblastoma SK-N-MC cells. Insulin sensitivity was evaluated by measuring insulin-stimulated Akt T308 phosphorylation and glucose uptake. We found that the phosphatase and tensin homologue deleted on chromosome 10 (PTEN) mediated Aβ-induced insulin resistance. Icariin treatment markedly reduced Aβ-enhanced PTEN protein levels, leading to an improvement in Aβ-induced insulin resistance. Accordingly, PTEN overexpression obviously abolished the protective effects of icariin on Aβ-induced insulin resistance. Furthermore, icariin activated proteasome activity. The proteasome inhibitor MG132 attenuated the effects of icariin on PTEN protein levels. Taken together, these results suggest that icariin protects SK-N-MC cells against Aβ-induced insulin resistance by activating the proteasome-dependent degradation of PTEN. These findings provide an experimental background for the identification of novel molecular targets of icariin, which may help in the development of alternative therapeutic approaches for neurodegenerative diseases.

Indexed as

amyloid-βicariininsulin resistanceneuronal cellsphosphatase and tensin homologue deleted on chromosome 10

Identifiers

PMID32581820
PMCPMC7296100
OpenAlexW3035466466

What OpenQuestion holds

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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.