Evidence map›Paper›PMID 30847744›Full record

ArticleInflammation2019

Sinomenine Attenuates Cartilage Degeneration by Regulating miR-223-3p/NLRP3 Inflammasome Signaling.

Hai-Chao Dong, Pei-Nan Li, Chang-Jian Chen, Xin Xu, Hong Zhang, Gang Liu, Lian-Jie Zheng, Peng Li

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
2.7field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 64 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

8 authors at 1 institution in 1 country.

Hai-Chao DongDepartment of Orthopedic Surgery, Second Clinical College, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, China. haic_dong@163.com.
Pei-Nan LiDepartment of Orthopedic Surgery, Second Clinical College, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, China.
Chang-Jian ChenDalian love cubic Health Management Co., Ltd, Dalian, 116000, China.
Xin XuDepartment of Orthopedic Surgery, Second Clinical College, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, China.
Hong ZhangDepartment of Orthopedic Surgery, Second Clinical College, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, China.
Gang LiuDepartment of Orthopedic Surgery, Second Clinical College, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, China.
Lian-Jie ZhengDepartment of Orthopedic Surgery, Second Clinical College, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, China.
Peng LiDepartment of Orthopedic Surgery, Second Clinical College, Dalian Medical University, No. 222 Zhongshan Road, Dalian, 116011, China.
Dalian Medical University · CN

Funding

the Medical Science Research Fund of Dalian City of China 1812021
6 · The paper itself

Abstract

Sinomenine (SIN) has been shown to protect against IL-1β-induced chondrocyte apoptosis in vitro. However, the role of SIN in the anterior cruciate ligament transection (ACLT)-induced osteoarthritis (OA) mouse model and its underlying molecular mechanisms remain unclear. In the present study, the protective effect of SIN on ACLT-induced articular cartilage degeneration and IL-1β-induced chondrocyte apoptosis miR-223-3p/NLRP3 signaling regulation was investigated. Safranin O staining was performed to evaluate the pathological changes of articular cartilage. Chondrocyte apoptosis was measured with Annexin V-fluorescein isothiocyanate/polyimide (annexin V-FITC/PI) staining using flow cytometry. Gene and protein expression were detected by RT-qPCR and Western blotting, respectively. SIN administration markedly improved articular cartilage degradation in mice undergoing ACLT surgery. In addition, SIN treatment downregulated the levels of inflammatory cytokines and the protein expression of NLRP3 inflammasome components and upregulated the expression of miR-223-3p in OA mice and IL-1β-stimulated chondrocytes. In vitro, we found that NLRP3 was a direct target of miR-223-3p, and overexpression of miR-223-3p blocked IL-1β-induced apoptosis and the inflammatory response in chondrocytes. These findings indicate that miR-223-3p/NLRP3 signaling could be used as a potential target of SIN for the treatment of OA.

Indexed as

AnimalsAntirheumatic AgentsCartilage, ArticularCartilage DiseasesGene Expression RegulationInflammasomesMiceMicroRNAsMorphinansNLR Family, Pyrin Domain-Containing 3 ProteinProtective AgentsSignal TransductionAntirheumatic AgentsInflammasomesMicroRNAsMIRN223 microRNA, mouseMorphinansNLR Family, Pyrin Domain-Containing 3 ProteinProtective AgentssinomeninechondrocytemiR-223-3pNLRP3osteoarthritissinomenine

Identifiers

PMID30847744
OpenAlexW2922222029

What OpenQuestion holds

Textmetadata
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.