Evidence map›Paper›PMID 32248810›Full record

ArticleJournal of neuroinflammation2020

Exogenous activation of cannabinoid-2 receptor modulates TLR4/MMP9 expression in a spinal cord ischemia reperfusion rat model.

Na Jing, Bo Fang, Zhe Li, Ayong Tian

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 89 citations in OpenAlex.

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  13. The mStem cell research & therapy · 2024
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  15. Alleviating CB2-Dependent ER Stress and Mitochondrial Dysfunction Improves Chronic Cerebral Hypoperfusion-Induced Cognitive Impairment.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024
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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

4 authors at 2 institutions in 1 country.

Na JingDepartment of Anesthesiology, First Affiliated Hospital, China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, People's Republic of China.
Bo FangDepartment of Anesthesiology, First Affiliated Hospital, China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, People's Republic of China.
Zhe LiDepartment of Anesthesiology, First Affiliated Hospital, China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, People's Republic of China.
Ayong TianDepartment of Anesthesiology, First Affiliated Hospital, China Medical University, 155 North Nanjing Street, Shenyang, 110001, Liaoning, People's Republic of China. tay0626@126.com.
China Medical University · CNFirst Hospital of China Medical University · CN

Funding

Natural Science Foundation of China 81971152
6 · The paper itself

Abstract

backgroundCannabinoid-2 receptor (CB2R) plays an important role in the cascading inflammation following ischemic injury. The toll-like receptors 4 (TLR4)/matrix metalloproteinase 9 (MMP9) signal pathway is involved in blood-brain barrier dysfunction induced by ischemia stroke. The aim of this study is to investigate the roles of exogenous activation of CB2R on attenuating neurological deficit and blood-spinal cord barrier (BSCB) disruption during rat spinal cord ischemia reperfusion (I/R) injury, through modulation of the TLR4/MMP9 axis.

methodsAnimals were intraperitoneally pretreated with TLR4 inhibitor TAK-242, CB2R agonist JWH-133 with or without CB2R antagonist AM630, or equivalent volume of vehicle 1 h before undergoing 14-min occlusion of descending aorta or sham operation. One, two, three, and 7 days after reperfusion, hindlimb locomotor function was evaluated with Basso, Beattie, and Bresnahan (BBB) Locomotor Scale, BSCB integrity was detected by measurement of Evans blue (EB) extravasation and spinal cord edema. The protein expression levels of CB2R, tight junction protein Zonula occluden-1 (ZO-1), TLR4, MMP9, MyD88, NF-κB p65, and NF-κB p-p65 were determined by western blot. The MMP9 activity was analyzed by gelatin zymography. Double immunofluorescence staining was used to identify the perivascular localization of CB2R, TLR4, MMP9, and reactive astrocytes, as well as the colocalization of CB2R, TLR4, and MMP9 with reactive astrocytes.

resultsJWH-133 pretreatment attenuated hindlimb motor functional deficit and BSCB leakage, along with preventing downregulation of ZO-1 and upregulation of TLR4/MMP9, similar to the effects of TAK-242 preconditioning. JWH-133 or TAK-242 pretreatment reduced the perivascular expression of TLR4/MMP9 and reactive astrocytes following injury. JWH-133 pretreatment also downregulated MyD88/NF-κB level, MMP9 activity, and the astrocytic TLR4/MMP9 after I/R injury.

conclusionsExogenous activation of CB2R by JWH-133 attenuated neurological deficit and BSCB disruption after spinal cord I/R injury via inhibition of TLR4/MMP9 expression.

Indexed as

AnimalsCannabinoidsDisease Models, AnimalDown-RegulationHindlimbMaleMatrix Metalloproteinase 9RatsRats, Sprague-DawleyReceptor, Cannabinoid, CB2Recovery of FunctionReperfusion InjurySignal TransductionSpinal CordSpinal Cord IschemiaSulfonamides1,1-dimethylbutyl-1-deoxy-Delta(9)-THCCannabinoidsethyl 6-(N-(2-chloro-4-fluorophenyl)sulfamoyl)cyclohex-1-ene-1-carboxylateMatrix Metalloproteinase 9Receptor, Cannabinoid, CB2SulfonamidesToll-Like Receptor 4AstrocyteBlood-spinal cord barrierCannabinoid-2 receptorIschemia reperfusionMMP9TLR4

Identifiers

PMID32248810
PMCPMC7132899
OpenAlexW3014118429

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.