Evidence map›Paper›PMID 33194078›Full record

ArticleAmerican journal of translational research2020

Morphine inhibits the promotion of inflammatory microenvironment on chronic tibial cancer pain through the PI3K-Akt-NF-κB pathway.

Diyang Ling, Yan Zhao, Zhenwu Zhang, Jiaya Li, Chunhui Zhu, Zheyin Wang

Open access · greenAbstract read
PubMed Full text at PMC
In one paragraph

Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

5 citing papers in PubMed, 5 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

6 authors at 1 institution in 1 country.

Diyang LingDepartment of Pain Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology) Shenzhen 518020, Guangdong, China.
Yan ZhaoDepartment of Pain Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology) Shenzhen 518020, Guangdong, China.
Zhenwu ZhangDepartment of Pain Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology) Shenzhen 518020, Guangdong, China.
Jiaya LiDepartment of Pain Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology) Shenzhen 518020, Guangdong, China.
Chunhui ZhuDepartment of Pain Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology) Shenzhen 518020, Guangdong, China.
Zheyin WangDepartment of Pain Medicine, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University, The First Affiliated Hospital, Southern University of Science and Technology) Shenzhen 518020, Guangdong, China.
Southern University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeInflammatory microenvironment is critical in the transmission of advanced cancer pain. This paper will study how morphine ameliorates advanced cancer pain through inflammatory microenvironment.

methodsFifty female healthy rats were selected and divided into control group, sham group, model group, morphine group and morphine + 740YP group by random number table. At the left tibia, rats in the model, morphine and morphine + 740YP groups received Walker256 cells injection, while those in the sham group received an equal amount of Hank solution. The control group received no treatment. After modeling, the rats' spontaneous pain behavior, paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured and statistically analyzed. The protein levels of PI3K, Akt, NF-κB and pro-inflammatory factors (TNF-α/IL-1β/IL-6/IL-17a) in rats were detected. Rat left dorsal root ganglion (DRG) cells were extracted and treated with 10, 20 and 30 μmol/L morphine to observe their effects on the cells.

resultsCompared with the control group, the model group presented increased spontaneous pain behavior and PWTL, decreased PWMT, and reduced mechanical pain threshold, as well as enhanced levels of PI3K, Akt, NF-κB and pro-inflammatory factors in vivo as compared to the control group. While the morphine group showed less spontaneous pain behavior and PWTL, increased PWMT, and down-regulated PI3K, Akt, NF-κB and pro-inflammatory factors in vivo in comparison with the model group. After morphine treatment, the apoptosis of DRG cells decreased and the cell activity increased, while PI3K, Akt, NF-κB and pro-inflammatory factors levels decreased. Morphine affected DRG cells in a dose-dependent manner. Up-regulation of PI3K could counteract the inhibitory effect of morphine on chronic tibial cancer pain.

conclusionsMorphine inhibits the promotion of inflammatory microenvironment on chronic tibial cancer pain via the PI3K/Akt/NF-κB pathway, and the regulation of the PI3K/Akt/NF-κB pathway can improve the therapeutic effect of morphine on chronic tibial cancer pain.

Indexed as

Chronic tibia cancer paininflammation microenvironmentmorphinePI3K-Akt-NF-κB pathway

Identifiers

PMID33194078
PMCPMC7653610
OpenAlexW3103868142

What OpenQuestion holds

Textmetadata
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Registered trials

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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.