Evidence map›Paper›PMID 31898189›Full record

ArticleSleep & breathing = Schlaf & Atmung2020

CB1 receptor antagonist rimonabant protects against chronic intermittent hypoxia-induced bone metabolism disorder and destruction in rats.

Zhan-Jun Dou, Xiao-Ling Gao, Yan-Li Jia, Jie Chen, Jiao-Jiao Yang, Yan Chen, Shu-Jie Wu, Tao Liu, Mei-Ting Wang, Chong Yang and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Sleep & breathing = Schlaf & Atmung, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 14 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

12 authors at 1 institution in 1 country.

Zhan-Jun DouDepartment of the Second Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Xiao-Ling GaoDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, No. 382, Wuyi Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Yan-Li JiaDepartment of Respiratory, Linfen Centrol Hospital, Linfen, Shanxi, People's Republic of China.
Jie ChenDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, No. 382, Wuyi Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Jiao-Jiao YangDepartment of the Second Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Yan ChenDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, No. 382, Wuyi Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Shu-Jie WuMedical Records Statistics Office, The First Hospital of Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Tao LiuDepartment of the Second Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Mei-Ting WangDepartment of the Second Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Chong YangDepartment of the Second Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Na ZhangDepartment of the Second Clinical Medicine, Shanxi Medical University, Taiyuan, Shanxi, People's Republic of China.
Bei WangDepartment of Respiratory and Critical Care Medicine, The Second Hospital of Shanxi Medical University, No. 382, Wuyi Road, Taiyuan, 030001, Shanxi, People's Republic of China. myemaila@qq.com.ORCID http://orcid.org/0000-0002-4771-5922
Shanxi Medical University · CN

Funding

Health and Family Planning Commission of Shanxi Province No. 2017048National Natural Science Foundation of China No. 81570086National Natural Science Foundation of China (CN) No. 81870076Shanxi Province Science and Technology Department No. 201703D421027Shanxi Scholarship Council of China No. 2017‑120Shanxi Scholarship Council of China No. 2017-Key 6
6 · The paper itself

Abstract

objectiveThe endocannabinoid system (ECS) regulates bone turn-over and remodeling. Chronic intermittent hypoxia (CIH) occurring during obstructive sleep apnea (OSA) may lead to disorders of the ECS and bone metabolism abnormalities. This study aimed to investigate whether or not the cannabinoid receptor 1 (CB1R) antagonist rimonabant (Ri) alleviates bone metabolism abnormalities and bone destruction induced by chronic intermittent hypoxia (CIH).

methodsHealthy male Sprague Dawley (SD) rats (n=48) were randomly divided into 6 groups of 8 rats: 2 normal control (NC) groups, 2 intermittent hypoxia (IH) groups, and 2 IH + Ri groups. Rats in NC groups breathed room air for 4 weeks (4w NC group) and 6 weeks (6w NC group). Rats in IH groups experienced IH environment for 4 weeks (4w IH group) and 6 weeks (6w IH group). In addition to the same IH exposure, rats in IH + Ri group were given daily intraperitoneal injection of Ri at the dosage of 1.5 mg/kg/d for 4 weeks (4w IH + Ri group) and 6 weeks (6w IH + Ri group). Levels of serum tartrate-resistant acid phosphatase (TRAP, a marker of bone resorption) were determined by ELISA. Hematoxylin and eosin (HE) staining was performed on bone sections to observe the changes in bone microstructure. Expression of CB1R in bone tissue was determined by immunohistochemistry.

resultsTRAP levels were higher in the 4w IH and 6w IH groups than in the 4w NC and 6w NC groups; TRAP levels were lower in the 4w IH + Ri and 6w IH + Ri groups than in the 4w IH and 6w IH groups. HE staining showed that the morphology of bone cells in the NC group was normal, but the 4w IH group had mild edema of bone cells, reduction in trabecular bone, and destruction of bone microstructure. Changes were more severe in the 6w IH group than 4w IH. The 4w IH + Ri group was slightly improved compared with the 4w IH group. The 6w IH + Ri group was improved compared with the 4w IH + Ri group. The results of immunohistochemistry showed that the expression of CB1R in IH group was significantly higher than that in NC group. The expression of CB1R in the IH + Ri group was lower than that in the IH group. With the prolongation of hypoxia, the expression of CB1R in bone cells of IH group increased. The expression level of CB1R in IH + Ri group decreased with the prolongation of intervention time. Correlation analysis showed that the expression rate of CB1R in bone cells was positively correlated with the level of TRAP in serum.

conclusionCIH increases serum TRAP levels and triggers metabolic bone disorder by activating bone CB1R. Intervention with CB1R antagonist (rimonabant) reduces the bone dysmetabolism in the CIH rat model.

Indexed as

AnimalsBone Diseases, MetabolicCannabinoid Receptor AntagonistsDisease Models, AnimalHypoxiaMaleOsteoclastsProtective AgentsRats, Sprague-DawleyReceptor, Cannabinoid, CB1RimonabantTartrate-Resistant Acid PhosphataseCannabinoid Receptor AntagonistsCnr1 protein, ratProtective AgentsReceptor, Cannabinoid, CB1RimonabantTartrate-Resistant Acid PhosphataseCannabinoid receptor 1 (CB1R)Chronic intermittent hypoxia (CIH)Obstructive sleep apnea syndrome (OSAS)Rimonabant (Ri)Tartrate-resistant acid phosphatase (TRAP)

Identifiers

PMID31898189
PMCPMC7679350
OpenAlexW2996978757

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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.