Evidence map›Paper›PMID 25452227›Full record

ArticleMolecular neurobiology2015

Posttreatment with 11-Keto-β-Boswellic Acid Ameliorates Cerebral Ischemia-Reperfusion Injury: Nrf2/HO-1 Pathway as a Potential Mechanism.

Yi Ding, MinChun Chen, MingMing Wang, YuWen Li, AiDong Wen

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.2field-weighted citation impact, top 3% 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

60 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
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  5. Toxicology reports · 2024
    Article
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  8. Review
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  11. Samarcandin protects against testicular ischemia/reperfusion injury in rats via activation of Nrf2/HO-1-mediated antioxidant responses.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2023
    Article
  12. Review
  13. Review
  14. Article
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  16. Review
  17. Review
  18. Article
  19. Article
  20. Induction of Heme Oxygenase-1 by 15d-Prostaglandin JAntioxidants (Basel, Switzerland) · 2022
    Article
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

5 authors at 2 institutions in 1 country.

Yi DingDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
MinChun ChenDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
MingMing WangDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, China.
YuWen LiDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, China. liyuwenzs@gmail.com.
AiDong WenDepartment of Pharmacy, Xijing Hospital, Fourth Military Medical University, Xi'an, China. adwen-2004@hotmail.com.
Air Force Medical University · CNXijing Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidative stress is well known to play a pivotal role in cerebral ischemia-reperfusion injury. 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. 11-Keto-β-boswellic acid (KBA) is a triterpenoid compound from extracts of Boswellia serrata. The aim of the present study was to determine whether KBA, a novel Nrf2 activator, can protect against cerebral ischemic injury. Middle cerebral artery occlusion (MCAO) was operated on male Sprague-Dawley rats. KBA (25 mg/kg) applied 1 h after reperfusion significantly reduced infarct volumes and apoptotic cells as well as increased neurologic scores at 48 h after reperfusion. Meanwhile, posttreatment with KBA significantly decreased malondialdehyde (MDA) levels, restored the superoxide dismutase (SOD) activity, and increased the protein Nrf2 and HO-1 expression in brain tissues. In primary cultured astrocytes, KBA increased the Nrf2 and HO-1 expression, which provided protection against oxygen and glucose deprivation (OGD)-induced oxidative insult. But knockdown of Nrf2 or HO-1 attenuated the protective effect of KBA. In conclusion, these findings provide evidence that the neuroprotection of KBA against oxidative stress-induced ischemic injury involves the Nrf2/HO-1 pathway.

Indexed as

AnimalsAntioxidantsApoptosisAstrocytesBoswelliaBrainBrain Damage, ChronicCell HypoxiaCells, CulturedDrug Evaluation, PreclinicalGlucoseHeme Oxygenase (Decyclizing)Infarction, Middle Cerebral ArteryMaleMalondialdehydeNerve Tissue Proteins11-keto-boswellic acidAntioxidantsGlucoseHeme Oxygenase (Decyclizing)Hmox1 protein, ratMalondialdehydeNerve Tissue ProteinsNeuroprotective AgentsNfe2l2 protein, ratNF-E2-Related Factor 2Superoxide DismutaseTriterpenes11-Keto-β-boswellic acidAntioxidantsHO-1MCAONrf2Oxygen glucose deprivation

Identifiers

PMID25452227
OpenAlexW1970552047

What OpenQuestion holds

Textmetadata
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.