Evidence map›Paper›PMID 26984336›Full record

ArticleJournal of molecular neuroscience : MN2016

Co-administration of 3-Acetyl-11-Keto-Beta-Boswellic Acid Potentiates the Protective Effect of Celecoxib in Lipopolysaccharide-Induced Cognitive Impairment in Mice: Possible Implication of Anti-inflammatory and Antiglutamatergic Pathways.

Aya Shoukry Sayed, Nesrine Salah El Dine El Sayed

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

13 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. The journey of boswellic acids from synthesis to pharmacological activities.Naunyn-Schmiedeberg's archives of pharmacology · 2024
    Review
  5. Acetyl-11-Keto-Evidence-based complementary and alternative medicine : eCAM · 2022
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. GenusIranian journal of basic medical sciences · 2020
    Review
  11. Review
  12. Article
  13. 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

2 authors at 2 institutions in 1 country.

Aya Shoukry SayedDepartment of Pharmaceutical Biology, Faculty of Pharmacy and Biotechnology, German University in Cairo, Main Entrance of Al Tagamoa Al Khames, New Cairo City, 11835, Egypt.
Nesrine Salah El Dine El SayedDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Giza, 12613, Egypt. nesrine.elsayed@guc.edu.eg.
Cairo University · EGGerman University in Cairo · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuro-inflammation is known to initiate the underlying pathogenesis of several neurodegenerative disorders which may progress to cognitive, behavioral, and functional impairment. Boswellia serrata is a well-known powerful anti-inflammatory agent used to treat several inflammatory diseases. The aim of the current study is to investigate the effect of the combination therapy of 3-acetyl-11-keto-β-boswellic acid (AKBA), a 5-lipoxygenase (5-LOX) inhibitor and celecoxib, and a selective cyclooxygenase-2 (COX-2) inhibitor as dual enzyme inhibitors compared to monotherapies with celecoxib and AKBA. Cognitive dysfunction is induced by intraperational injection of lipopolysaccharide (LPS) in mice. Radial maze, Y maze, and novel object recognition (NOR) were performed to evaluate the possible behavioral changes. Moreover, estimation of glutamate and tumor necrosis factor-alpha (TNF-α), as well as an immunohistochemical investigation of amyloid beta peptide (Aβ) was performed to evaluate the molecular changes that followed the LPS or drug treatment. The results showed that the combination therapy of AKBA and celecoxib reversed the behavioral and molecular changes caused by LPS cognitive dysfunction model that predispose cognitive dysfunction in mice. This study showed the effectiveness of the dual therapy with AKBA and celecoxib as anti-inflammatory, antiglutamatergic, and anti-amyloidogenic agents in the management of cognitive dysfunction.

Indexed as

Amyloid beta-PeptidesAnimalsAnti-Inflammatory AgentsCelecoxibCognitive DysfunctionCyclooxygenase 2 InhibitorsDrug CombinationsDrug SynergismGlutamic AcidLipopolysaccharidesLipoxygenase InhibitorsMaleMiceTriterpenesTumor Necrosis Factor-alphaacetyl-11-ketoboswellic acidAmyloid beta-PeptidesAnti-Inflammatory AgentsCelecoxibCyclooxygenase 2 InhibitorsDrug CombinationsGlutamic AcidLipopolysaccharidesLipoxygenase InhibitorsTriterpenesTumor Necrosis Factor-alpha3-Acetyl-11-keto-β-boswellic acidAmyloid beta peptideCognitive dysfunctionGlutamateLipopolysaccharideTumor necrosis factor-alpha

Identifiers

PMID26984336
OpenAlexW2324220434

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.