Evidence map›Paper›PMID 25384416›Full record

ArticleScientific reports2014

Neuroprotection by acetyl-11-keto-β-Boswellic acid, in ischemic brain injury involves the Nrf2/HO-1 defense pathway.

Yi Ding, MinChun Chen, Min Wang, MingMing Wang, Tiejun Zhang, Jongsun Park, YanRong Zhu, Chao Guo, YanYan Jia, YuWen Li and 1 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
11.8field-weighted citation impact, top 1% 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

79 citing papers in PubMed, 156 citations in OpenAlex.

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  15. The journey of boswellic acids from synthesis to pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  16. Impact of NQO1 dysregulation in CNS disorders.Journal of translational medicine · 2024
    Review
  17. Review
  18. Article
  19. Article
  20. Article

19 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 2 countries.

Yi DingDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
MinChun ChenDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
Min WangDepartment of Pharmacology, School of Pharmacy, Fourth Military Medical University.
MingMing WangDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
Tiejun ZhangDepartment of Pharmacology, Chungnam National University.
Jongsun ParkDepartment of Pharmacology, Chungnam National University.
YanRong ZhuDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
Chao GuoDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
YanYan JiaDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
YuWen LiDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
AiDong WenDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University.
Air Force Medical University · CNChungnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stroke is a complex disease involved oxidative stress-related pathways in its pathogenesis. The nuclear factor erythroid-2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway has been considered a potential target for neuroprotection in stroke. Acetyl-11-Keto-β-Boswellic Acid (AKBA) is an active triterpenoid compound from the extract of Boswellia serrate. The present study was to determine whether AKBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. The stroke model was produced in Sprague-Dawley rats via middle cerebral artery occlusion. To model ischemia-like conditions in vitro, primary cultured cortical neurons were exposed to transient oxygen and glucose deprivation (OGD). Treatment of AKBA significantly reduced infarct volumes and apoptotic cells, and also increased neurologic scores by elevating the Nrf2 and HO-1 expression in brain tissues in middle cerebral artery occlusion (MCAO) rats at 48 hours post reperfusion. In primary cultured neurons, AKBA increased the Nrf2 and HO-1 expression, which provided protection against OGD-induced oxidative insult. Additionally, AKBA treatment increased Nrf2 binding activity to antioxidant-response elements (ARE). The protective effect of AKBA was attenuated by knockdown of Nrf2 or HO-1. In conclusion, these findings provide evidence that AKBA protects neurons against ischemic injury, and this neuroprotective effect involves the Nrf2/HO-1 pathway.

Indexed as

AnimalsAntioxidant Response ElementsApoptosisBrain IschemiaCell HypoxiaCerebral CortexDisease Models, AnimalGene Expression RegulationGlucoseHeme Oxygenase-1MaleNeuronsNeuroprotective AgentsNF-E2-Related Factor 2OxygenPrimary Cell Cultureacetyl-11-ketoboswellic acidGlucoseHeme Oxygenase-1Neuroprotective AgentsNfe2l2 protein, ratNF-E2-Related Factor 2OxygenRNA, Small InterferingTriterpenes

Identifiers

PMID25384416
PMCPMC4227012
OpenAlexW2065716130

What OpenQuestion holds

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LicenceCC BY
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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.