Evidence map›Paper›PMID 35463083›Full record

ArticleEvidence-based complementary and alternative medicine : eCAM2022

Inhibition of PDE10A-Rescued TBI-Induced Neuroinflammation and Apoptosis through the cAMP/PKA/NLRP3 Pathway.

Jin Huang, Dang Tang, Yiqiang Cao, Yonggang Wang, Jiang Long, Lin Wei, Hai Song

Open access · hybridAbstract read
In one paragraph

Article in Evidence-based complementary and alternative medicine : eCAM, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.9field-weighted citation impact, top 30% 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

3 citing papers in PubMed, 10 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

7 authors at 1 institution in 1 country.

Jin HuangDepartment of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Dang TangDepartment of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Yiqiang CaoDepartment of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Yonggang WangDepartment of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Jiang LongDepartment of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Lin WeiDepartment of Ultrasound, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.
Hai SongDepartment of Neurosurgery, First Affiliated Hospital of Kunming Medical University, Kunming 650032, China.ORCID https://orcid.org/0000-0003-2119-6439
Kunming Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Phosphodiesterase 10A (PDE10A) is a dual-substrate phosphodiesterase that is highly expressed in the striatal complex. PDE10A is an important target for the treatment of ganglion dysfunction and neuroinflammation-related diseases, but its possible impact on traumatic brain injury (TBI) is still unclear. This study aims to investigate the protective effects of inhibiting PDE10A on neuroinflammation post-TBI injury and its possible molecular mechanism. The expression of PDE10A in rats and HT22 cells was determined by Western blotting. The neurological dysfunction of these rats was detected by Nissl staining, hematoxylin-eosin (HE) staining, and Morris water maze test. The activity of HT22 cells was measured by MTT. The findings of this study suggest that PDE10A is highly expressed in the brain tissue of TBI rats and HT22 cells induced by mechanical injury. Inhibition of PDE10A reduces the expression of interleukin-1

Identifiers

PMID35463083
PMCPMC9019408
OpenAlexW4223594627

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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.