Evidence map›Paper›PMID 32677362›Full record

ArticleJournal of cellular and molecular medicine2020

Neuroprotective effects of 1-O-hexyl-2,3,5-trimethylhydroquinone on ischaemia/reperfusion-induced neuronal injury by activating the Nrf2/HO-1 pathway.

Chaoliang Tang, Yida Hu, Haiyan Lyu, Jie Gao, Jiazhen Jiang, Xiude Qin, Yuanbo Wu, Jiawu Wang, Xiaoqing Chai

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 14 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

9 authors at 6 institutions in 2 countries.

Chaoliang TangDepartment of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.ORCID 0000-0002-1936-028X
Yida HuDepartment of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, China.
Haiyan LyuDepartment of Neurology, Shanghai General Hospital, Shanghai Jiao Tong University, Shanghai, China.
Jie GaoDepartment of Anesthesia, Critical Care & Pain Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Jiazhen JiangDepartment of Emergency, Huashan Hospital North, Fudan University, Shanghai, China.
Xiude QinDepartment of Neurology, Shenzhen Traditional Chinese Medicine Hospital, The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine, Shenzhen, China.
Yuanbo WuDepartment of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Jiawu WangDepartment of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
Xiaoqing ChaiDepartment of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, China.
University of Science and Technology of China · CNFudan University · CNGuangzhou University of Chinese Medicine · CNHarvard University · USShanghai Jiao Tong University · CNWuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1-O-Hexyl-2,3,5-trimethylhydroquinone (HTHQ), a lipophilic phenolic agent, has an antioxidant activity and reactive oxygen species (ROS) scavenging property. However, the role of HTHQ on cerebral ischaemic/reperfusion (I/R) injury and the underlying mechanisms remain poorly understood. In the present study, we demonstrated that HTHQ treatment ameliorated cerebral I/R injury in vivo, as demonstrated by the decreased infarct volume ration, neurological deficits, oxidative stress and neuronal apoptosis. HTHQ treatment increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant protein, haeme oxygenase-1 (HO-1). In addition, HTHQ treatment decreases oxidative stress and neuronal apoptosis of PC12 cells following hypoxia and reperfusion (H/R) in vitro. Moreover, we provided evidence that PC12 cells were more vulnerable to H/R-induced oxidative stress after si-Nrf2 transfection, and the HTHQ-mediated protection was lost in PC12 cells transfected with siNrf2. In conclusion, these results suggested that HTHQ possesses neuroprotective effects against oxidative stress and apoptosis after cerebral I/R injury via activation of the Nrf2/HO-1 pathway.

Indexed as

Signal TransductionAnimalsAntioxidantsApoptosisHeme Oxygenase-1HydroquinonesMaleMice, Inbred C57BLNeuronsNeuroprotective AgentsNF-E2-Related Factor 2Oxidative StressPC12 CellsRatsReperfusion Injury1-O-hexyl-2,3,5-trimethylhydroquinoneAntioxidantsHeme Oxygenase-1HydroquinonesNeuroprotective AgentsNF-E2-Related Factor 21-O-Hexyl-2,3,5-trimethylhydroquinonecerebral ischaemic/reperfusionHO-1Nrf2PC12 cells

Identifiers

PMID32677362
PMCPMC7521305
OpenAlexW3043005241

What Socratic 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 Socratic graph.