Evidence map›Paper›PMID 27087648›Full record

ArticleNeuromolecular medicine2016

Trans-Cinnamaldehyde, An Essential Oil in Cinnamon Powder, Ameliorates Cerebral Ischemia-Induced Brain Injury via Inhibition of Neuroinflammation Through Attenuation of iNOS, COX-2 Expression and NFκ-B Signaling Pathway.

Yuh-Fung Chen, Yu-Wen Wang, Wei-Shih Huang, Ming-Ming Lee, W Gibson Wood, Yuk-Man Leung, Huei-Yann Tsai

Abstract read
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In one paragraph

Article in Neuromolecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Review
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  14. Polysaccharide derived fromAmerican journal of translational research · 2022
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  15. Inhalation AromatherapyFrontiers in pharmacology · 2022
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  19. The Extracts ofOxidative medicine and cellular longevity · 2021
    Article
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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.

Yuh-Fung ChenDepartment of Pharmacology, China Medical University, 91 Hsueh-Shih Road, Taichung, 40402, Taiwan. yfchen@mail.cmu.edu.tw.
Yu-Wen WangDepartment of Chinese Pharmaceutical Sciences and Chinese Medicine Resources, China Medical University, Taichung, 40402, Taiwan.
Wei-Shih HuangDepartment of Neurology, China Medical University, Taichung, 40402, Taiwan.
Ming-Ming LeeDepartment of Health and Nutrition Biotechnology, Asia University, Taichung, 41354, Taiwan.
W Gibson WoodDepartment of Pharmacology, Geriatric Research, Education and Clinical Center VA Medical Center, University of Minnesota, Minneapolis, MN, 55455, USA.
Yuk-Man LeungDepartment of Physiology, China Medical University, Taichung, 40402, Taiwan.
Huei-Yann TsaiDepartment of Pharmacy, China Medical University Hospital, Taichung, 40447, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trans-cinnamaldehyde (TCA), an essential oil in cinnamon powder, may have beneficial effects as a treatment for stroke which is the second leading cause of death worldwide. Post-ischemic inflammation induces neuronal cell damage after stroke, and activation of microglia, in particular, has been thought as the main contributor of proinflammatory and neurotoxic factors. The purpose of this study was to investigate the neuroprotective effects of TCA in an animal model of ischemia/reperfusion (I/R)-induced brain injury and the neuroprotective mechanism was verified in LPS-induced inflammation of BV-2 microglial cells. Our results showed that TCA (10-30 mg/kg, p.o.) significantly reduced the infarction area, neurological deficit score and decreased iNOS and COX-2 protein expression level in I/R-induced injury brain tissue. It inhibited 0.5 µg/ml LPS-induced NO production in BV-2 microglial cells without affecting cell viability, reduced protein expression of iNOS and COX-2, and attenuated inhibition of p53 protein. TCA also suppressed the effects of LPS-induced nuclear translocation of NF-κB p65 and p50 and increased cytosolic IκBα. It also reduced LPS-induced mRNA expression of iNOS, COX-2, and TNFα. We concluded that TCA has a potential neuroprotective effect to against the ischemic stroke, which may be via the inhibition of neuroinflammation through attenuating iNOS, COX-2 expression and NF-κB signaling pathway.

Indexed as

AcroleinAnimalsBrain InjuriesBrain IschemiaCinnamomum zeylanicumCyclooxygenase 2Disease Models, AnimalGene Expression RegulationInflammationMicrogliaNF-kappa BNitric Oxide Synthase Type IIAcroleincinnamaldehydeCyclooxygenase 2NF-kappa BNitric Oxide Synthase Type IIBV-2 microgliaCerebral ischemiaNeuroinflammationNF-κB signaling pathwayTrans-cinnamaldehyde

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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.