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Article

Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity

  • Authors:
    • Anum Jamil
    • Aamra Mahboob
    • Touqeer Ahmed
  • View Affiliations / Copyright

    Affiliations: Neurobiology Laboratory, Atta‑ur‑Rahman School of Applied Biosciences, National University of Sciences and Technology, Sector H‑12, Islamabad 44000, Pakistan
  • Pages: 601-606
    |
    Published online on: December 10, 2015
       https://doi.org/10.3892/etm.2015.2928
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Abstract

Aluminum is known to exert neurotoxic effects associated with various neurodegenerative disorders, including Alzheimer's disease (AD). Ibuprofen is a well‑known non‑steroidal anti‑inflammatory drug, which has demonstrated potential efficacy in the treatment of numerous inflammatory and neurodegenerative disorders, including AD. The present study aimed to investigate the protective effects of ibuprofen on cognitive function, and the expression levels of neuronal pentraxins (NPs) and interleukin (IL)‑1β in an aluminum chloride (AlCl3)‑induced mouse model of neurotoxicity. The effects of ibuprofen (100 mg/kg/day for 12 days) on learning and memory were evaluated in the AlCl3‑induced neurotoxic mice using a Morris water maze and open field tests. In addition, ibuprofen was assessed for its effects on the expression levels of NPs and IL‑1β in the hippocampus, cortex and amygdala of the brain. Treatment of the AlCl3‑treated mice with ibuprofen decreased anxiety levels (6.90±0.34 min) compared with the AlCl3‑treated group (1.80±0.29 min), as indicated by the time spent in the central area in an open field test. Furthermore, the expression levels of NP1 (1.32±0.47) and IL‑1β (0.99±0.21) were significantly decreased in the hippocampus of mice following ibuprofen treatment, as compared with the AlCl3‑treated mice (8.62±1.54 and 7.47±0.53, respectively). In the present study, ibuprofen was able to target novel structures in order to attenuate the inflammation associated with an AlCl3‑induced mouse model of neurotoxicity; thus suggesting that ibuprofen may be considered a potential therapeutic option for the treatment of neurodegenerative diseases, including AD.
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Copy and paste a formatted citation
Spandidos Publications style
Jamil A, Mahboob A and Ahmed T: Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity. Exp Ther Med 11: 601-606, 2016.
APA
Jamil, A., Mahboob, A., & Ahmed, T. (2016). Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity. Experimental and Therapeutic Medicine, 11, 601-606. https://doi.org/10.3892/etm.2015.2928
MLA
Jamil, A., Mahboob, A., Ahmed, T."Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity". Experimental and Therapeutic Medicine 11.2 (2016): 601-606.
Chicago
Jamil, A., Mahboob, A., Ahmed, T."Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity". Experimental and Therapeutic Medicine 11, no. 2 (2016): 601-606. https://doi.org/10.3892/etm.2015.2928
Copy and paste a formatted citation
x
Spandidos Publications style
Jamil A, Mahboob A and Ahmed T: Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity. Exp Ther Med 11: 601-606, 2016.
APA
Jamil, A., Mahboob, A., & Ahmed, T. (2016). Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity. Experimental and Therapeutic Medicine, 11, 601-606. https://doi.org/10.3892/etm.2015.2928
MLA
Jamil, A., Mahboob, A., Ahmed, T."Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity". Experimental and Therapeutic Medicine 11.2 (2016): 601-606.
Chicago
Jamil, A., Mahboob, A., Ahmed, T."Ibuprofen targets neuronal pentraxins expresion and improves cognitive function in mouse model of AlCl3‑induced neurotoxicity". Experimental and Therapeutic Medicine 11, no. 2 (2016): 601-606. https://doi.org/10.3892/etm.2015.2928
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