Evidence map›Paper›PMID 39080620›Full record

ArticleBMC musculoskeletal disorders2024

Liraglutide, a glucagon-like peptide-1 receptor agonist, ameliorates inflammation and apoptosis via inhibition of receptor for advanced glycation end products signaling in AGEs induced chondrocytes.

Xianyu Zhang, Jian Jiang, Jiajia Xu, Jian Chen, Yuntao Gu, Guobao Wu

Abstract read
In one paragraph

Article in BMC musculoskeletal disorders, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

23 citing papers in PubMed, 1 synthesis or guideline 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

6 authors.

Xianyu ZhangDepartment of Orthopedics, ShangRao People's Hospital, Shangrao, Jiangxi province, 334000, China.
Jian JiangDepartment of Orthopedics, ShangRao People's Hospital, Shangrao, Jiangxi province, 334000, China.
Jiajia XuDepartment of Orthopedics, ShangRao People's Hospital, Shangrao, Jiangxi province, 334000, China.
Jian ChenDepartment of Orthopedics, ShangRao People's Hospital, Shangrao, Jiangxi province, 334000, China.
Yuntao GuSpine Surgery, The Second Affiliated Hospital of Hainan Medical University, 368 Yehai Dadao, Longhua District, Haikou, Hainan, 570216, China. 18608956606@163.com.
Guobao WuDepartment of Orthopedics, ShangRao People's Hospital, Shangrao, Jiangxi province, 334000, China. wu900808@126.com.

Funding

Science and Technology Plan of Jiangxi Provincial Health Commission SKJP220218860
6 · The paper itself

Abstract

backgroundThis study aimed to investigate functions of GLP-1R agonist by liraglutide (LIRA) and revealing the mechanism related to AGEs/RAGE in chondrocytes.

methodsTo illustrate potential effect of GLP-1R agonist on AGEs induced chondrocytes, chondrocytes were administrated by AGEs with LIRA and GLP-1R inhibitor exendin. Inflammatory factors were assessed using ELISA. Real-time PCR was used to evaluate the catabolic activity MMPs and ADAMTS mRNA level, as well as anabolic activity (aggrecan and collagen II). RAGE expression was investigated by Western blotting. TUNEL, caspase3 activity and immunofluorescence were performed to test the apoptotic activity.

resultsOur results showed that treatment with LIRA at > 100 nM attenuated the AGE-induced chondrocyte viability. Western bolt demonstrated that GLP-1R activation by LIRA treatment reduced RAGE protein expression compared with the AGEs groups. ELISA showed that LIRA hindered the AGEs-induced production of inflammatory cytokines (IL-6, IL-12 and TNF-α) in primary chondrocytes. AGEs induced catabolism levels (MMP-1, -3, -13 and ADAMTS-4, 5) are also attenuated by LIRA, causing the retention of more extracellular matrix (Aggrecan and Collagen II). TUNEL, caspase3 activity and immunofluorescence results indicated that LIRA inhibited the AGEs-induced production of inflammatory cytokines in primary chondrocytes and attenuated the caspase 3 level, leading to the reduced apoptotic activity. All the protective effects are reversed by exendin (GLP-1R blockers).

conclusionsThe present study demonstrates for the first time that LIRA, an agonist for GLP-1R which is commonly used in type 2 diabetes reverses AGEs induced chondrocyte inflammation and apoptosis through suppressing RAGE signaling, contributing to reduced catabolism and retention of more extracellular matrix. The above results indicate the possible effect of GLP-1R agonist on treating OA.

Indexed as

ApoptosisChondrocytesGlycation End Products, AdvancedLiraglutideSignal TransductionAnimalsCells, CulturedCytokinesGlucagon-Like Peptide-1 ReceptorInflammationMaleRatsRats, Sprague-DawleyCytokinesGlucagon-Like Peptide-1 ReceptorGlycation End Products, AdvancedLiraglutideAGEsGLP-1RLiraglutideOsteoarthritisRAGE

Identifiers

PMID39080620
PMCPMC11287913

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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.