Evidence map›Paper›PMID 29968707›Full record

ArticleExperimental & molecular medicine2018

Modulation of M1/M2 polarization by capsaicin contributes to the survival of dopaminergic neurons in the lipopolysaccharide-lesioned substantia nigra in vivo.

Eugene Bok, Young Cheul Chung, Ki-Suk Kim, Hyung Hwan Baik, Won-Ho Shin, Byung Kwan Jin

Open access · goldAbstract read
In one paragraph

Article in Experimental & molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 4% 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

70 citing papers in PubMed, 1 synthesis or guideline pooled it, 121 citations in OpenAlex.

  1. A Systematic Review of the Effects of Capsaicin on Alzheimer's Disease.International journal of molecular sciences · 2023
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10 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Eugene BokPredictive Model Research Center, Korea Institute of Toxicology, Daejeon, 34114, Korea.
Young Cheul ChungDepartment of Biochemistry and Molecular Biology, School of Medicine Kyung Hee University, Seoul, 02447, Korea.
Ki-Suk KimPredictive Model Research Center, Korea Institute of Toxicology, Daejeon, 34114, Korea.
Hyung Hwan BaikDepartment of Biochemistry and Molecular Biology, School of Medicine Kyung Hee University, Seoul, 02447, Korea.
Won-Ho ShinPredictive Model Research Center, Korea Institute of Toxicology, Daejeon, 34114, Korea. whshin@kitox.re.kr.
Byung Kwan JinDepartment of Biochemistry and Molecular Biology, School of Medicine Kyung Hee University, Seoul, 02447, Korea. bkjin@khu.ac.kr.
Korea Institute of Toxicology · KRKyung Hee University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study examined the neuroprotective effects of capsaicin (CAP) and explored their underlying mechanisms in a lipopolysaccharide (LPS)-lesioned inflammatory rat model of Parkinson's dieases (PD). LPS was unilaterally injected into the substantia nigra (SN) in the absence or presence of CAP or capsazepine (CZP, a TRPV1 antagonist). The SN tissues were prepared for immunohistochemical staining, reverse transcriptase-polymerase chain reaction (RT-PCR) analysis, western blot analysis, blood-brain barrier (BBB) permeability evaluation, and reactive oxygen species (ROS) detection. We found that CAP prevented the degeneration of nigral dopamine neurons in a dose-dependent manner and inhibited the expression of proinflammatory mediators in the LPS-lesioned SN. CAP shifted the proinflammatory M1 microglia/macrophage population to an anti-inflammatory M2 state as demonstrated by decreased expression of M1 markers (i.e., inducible nitric oxide synthase; iNOS and interleukin-6) and elevated expression of M2 markers (i.e., arginase 1 and CD206) in the SN. RT-PCR, western blotting, and immunohistochemical analysis demonstrated decreased iNOS expression and increased arginase 1 expression in the CAP-treated LPS-lesioned SN. Peroxynitrate production, reactive oxygen species levels and oxidative damage were reduced in the CAP-treated LPS-lesioned SN. The beneficial effects of CAP were blocked by CZP, indicating TRPV1 involvement. The present data indicate that CAP regulated the M1 and M2 activation states of microglia/macrophage in the LPS-lesioned SN, which resulted in the survival of dopamine neurons. It is therefore likely that TRPV1 activation by CAP has therapeutic potential for treating neurodegenerative diseases, that are associated with neuroinflammation and oxidative stress, such as PD.

Indexed as

AnimalsArginaseCapsaicinCell DifferentiationDopaminergic NeuronsInterleukin-6Lectins, C-TypeLipopolysaccharidesMacrophagesMannose-Binding LectinsMannose ReceptorMicrogliaNeuroprotective AgentsNitric Oxide Synthase Type IIOxidative StressParkinson DiseaseArginaseCapsaicinInterleukin-6Lectins, C-TypeLipopolysaccharidesMannose-Binding LectinsMannose ReceptorNeuroprotective AgentsNitric Oxide Synthase Type IIReceptors, Cell SurfaceTrpv1 protein, ratTRPV Cation Channels

Identifiers

PMID29968707
PMCPMC6030094
OpenAlexW2809899329

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.