Evidence map›Paper›PMID 31383790›Full record

ArticleBioscience reports2019

Liraglutide inhibits the apoptosis of human nucleus pulposus cells induced by high glucose through PI3K/Akt/caspase-3 signaling pathway.

Yao Ming-Yan, Zhang Jing, Guo Shu-Qin, Bai Xiao-Liang, Li Zhi-Hong, Zhou Xue

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 26 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

6 authors at 2 institutions in 1 country.

Yao Ming-YanDepartment of Endocrinology, Baoding NO.1 Central Hospital, 320 Changcheng North Street, Lianchi District, Baoding City, Hebei Province, China.
Zhang JingDepartment of Cardiology, Affiliated Hospital of Hebei University, Baoding City, Hebei Province, China.
Guo Shu-QinDepartment of Endocrinology, Baoding NO.1 Central Hospital, 320 Changcheng North Street, Lianchi District, Baoding City, Hebei Province, China.
Bai Xiao-LiangDepartment of Endocrinology, Baoding NO.1 Central Hospital, 320 Changcheng North Street, Lianchi District, Baoding City, Hebei Province, China.
Li Zhi-HongDepartment of Endocrinology, Baoding NO.1 Central Hospital, 320 Changcheng North Street, Lianchi District, Baoding City, Hebei Province, China lizhihongmd@163.com.ORCID 0000-0003-1010-2628
Zhou XueDepartment of Endocrinology, Baoding NO.1 Central Hospital, 320 Changcheng North Street, Lianchi District, Baoding City, Hebei Province, China.
Baoding No.1 Central HospitalAffiliated Hospital of Hebei University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes mellitus (DM) is a potential etiology of disc degeneration. Glucagon-like peptide-1 (GLP-1) is currently regarded as a powerful treatment option for type 2 diabetes. Apart from the beneficial effects on glycaemic control, GLP-1 has been reported to exert functions in a variety of tissues on modulation of cell proliferation, differentiation, and apoptosis. However, little is known regarding the effects of GLP-1 on nucleus pulposus cells (NPCs). In the present study, we investigated the effects of liraglutide (LIR), a long-lasting GLP-1 analogue, on apoptosis of human NPCs and the underlying mechanisms involved. We confirmed the presence of GLP-1 receptor (GLP-1R) in NPCs. Our data demonstrated that liraglutide inhibited the apoptosis of NPCs induced by high glucose (HG), as detected by Annexin V/Propidium Iodide (PI) and ELISA assays. Moreover, liraglutide down-regulated caspase-3 activity at intermediate concentration (100 nM) for maximum effect. Further analysis suggested that liraglutide suppressed reactive oxygen species (ROS) generation and stimulated the phosphorylation of Akt under HG condition. Pretreatment of cells with the Phosphoinositide 3-kinase (PI3K) inhibitor LY294002 (LY) and small interfering RNAs (siRNAs) GLP-1R abrogated the liraglutide-induced activation of Akt and the protective effects on NPCs' apoptosis. In conclusion, liraglutide could directly protect NPCs against HG-induced apoptosis by inhibiting oxidative stress and activate the PI3K/Akt/caspase-3 signaling pathway via GLP-1R.

Indexed as

ApoptosisCaspase 3Cells, CulturedDiabetes ComplicationsGlucoseHumansIntervertebral Disc DegenerationLiraglutideNucleus PulposusPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionCASP3 protein, humanCaspase 3GlucoseLiraglutidePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktapoptosisliraglutidenucleus pulposus cellsoxidative stresssignaling pathway

Identifiers

PMID31383790
PMCPMC6702359
OpenAlexW2965882949

What OpenQuestion holds

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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.