Evidence map›Paper›PMID 28814985›Full record

ArticleOxidative medicine and cellular longevity2017

Activation of Endocannabinoid Receptor 2 as a Mechanism of Propofol Pretreatment-Induced Cardioprotection against Ischemia-Reperfusion Injury in Rats.

Hai-Jing Sun, Yan Lu, Hao-Wei Wang, Hao Zhang, Shuang-Ran Wang, Wen-Yun Xu, Hai-Long Fu, Xue-Ya Yao, Feng Yang, Hong-Bin Yuan

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2017. 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
2.6field-weighted citation impact, top 10% 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, 33 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

10 authors at 4 institutions in 1 country.

Hai-Jing SunDepartment of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China.
Yan LuDepartment of Neurology, PLA Rocket Force General Hospital, No. 16 Xinjiekouwai Street, Beijing 100088, China.
Hao-Wei WangDepartment of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China.
Hao ZhangDepartment of Anesthesiology, PLA Rocket Force General Hospital, No. 16 Xinjiekouwai Street, Beijing 100088, China.ORCID 0000-0001-5624-9217
Shuang-Ran WangNursing School of Shanghai Jiguang Polytechnic College, No. 2859 Shuichan Road, Shanghai 201901, China.
Wen-Yun XuDepartment of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China.
Hai-Long FuDepartment of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China.
Xue-Ya YaoHebei North University School of Medicine, Zhangjiakou, Hebei 075000, China.
Feng YangSchool of Pharmacy, Second Military Medical University, No. 325 Guohe Road, Shanghai 200433, China.ORCID 0000-0001-5164-5413
Hong-Bin YuanDepartment of Anesthesiology, Changzheng Hospital Affiliated to Second Military Medical University, No. 415 Fengyang Road, Shanghai 200003, China.ORCID 0000-0001-6447-2961
Second Military Medical University · CNAir Force General Hospital PLA · CNHebei North University · CNShanghai Polytechnic University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Propofol pretreatment before reperfusion, or propofol conditioning, has been shown to be cardioprotective, while its mechanism is unclear. The current study investigated the roles of endocannabinoid signaling in propofol cardioprotection in an in vivo model of myocardial ischemia/reperfusion (I/R) injury and in in vitro primary cardiomyocyte hypoxia/reoxygenation (H/R) injury. The results showed that propofol conditioning increased both serum and cell culture media concentrations of endocannabinoids including anandamide (AEA) and 2-arachidonoylglycerol (2-AG) detected by LC-MS/MS. The reductions of myocardial infarct size in vivo and cardiomyocyte apoptosis and death in vitro were accompanied with attenuations of oxidative injuries manifested as decreased reactive oxygen species (ROS), malonaldehyde (MDA), and MPO (myeloperoxidase) and increased superoxide dismutase (SOD) production. These effects were mimicked by either URB597, a selective endocannabinoids degradation inhibitor, or VDM11, a selective endocannabinoids reuptake inhibitor. In vivo study further validated that the cardioprotective and antioxidative effects of propofol were reversed by selective CB2 receptor antagonist AM630 but not CB1 receptor antagonist AM251. We concluded that enhancing endogenous endocannabinoid release and subsequent activation of CB2 receptor signaling represent a major mechanism whereby propofol conditioning confers antioxidative and cardioprotective effects against myocardial I/R injury.

Indexed as

AnimalsApoptosisArachidonic AcidsBenzamidesCarbamatesCells, CulturedEndocannabinoidsIndolesMaleMalondialdehydeMyocardial Reperfusion InjuryMyocytes, CardiacPentobarbitalPeroxidasePropofolRatsArachidonic AcidsBenzamidesCarbamatescyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl esterEndocannabinoidsIndolesiodopravadolineMalondialdehydeN-(2-methyl-3-hydroxyphenyl)-5,8,11,14-eicosatetraenamidePentobarbitalPeroxidasePropofolReactive Oxygen SpeciesReceptor, Cannabinoid, CB1Receptor, Cannabinoid, CB2Superoxide Dismutase

Identifiers

PMID28814985
PMCPMC5549482
OpenAlexW2736976401

What OpenQuestion holds

Textmetadata
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.