The brain consequences of systemic inflammation were not fully alleviated by ibuprofen treatment in mice.


Journal

Pharmacological reports : PR
ISSN: 2299-5684
Titre abrégé: Pharmacol Rep
Pays: Switzerland
ID NLM: 101234999

Informations de publication

Date de publication:
Feb 2021
Historique:
received: 13 03 2020
accepted: 15 07 2020
revised: 13 07 2020
pubmed: 23 7 2020
medline: 9 9 2021
entrez: 23 7 2020
Statut: ppublish

Résumé

Extensive data point to the immune system as an important factor underlying the pathogenesis of brain diseases. Epidemiological studies have shown that long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs) significantly reduces the onset and progression of Alzheimer's disease. The present study aimed to investigate whether ibuprofen (IBU) is able to prevent the long-lasting alterations of brain function induced by systemic inflammation. Mice received intraperitoneal injections of lipopolysaccharide (LPS; 250 µg/kg/day) for seven consecutive days. Ibuprofen administration (40 mg/kg/day) was started three days before the LPS injections and continued until the last day of LPS injection. Within the next 2 weeks, mice performances on the behavioral tests were evaluated, and then brain tissue samples for biochemical analyses were collected. The findings showed that ibuprofen significantly improved mice's performance in the passive avoidance test and reduced anxiety- and depressive-like behaviors. However, ibuprofen could not significantly improve spatial memory in the Morris water maze test and recognition ability in the novel object recognition test. TNF-α and IL-1β cytokines levels and malondialdehyde (MDA) concentration in the hippocampal tissues of LPS-treated mice were significantly lowered by ibuprofen treatment, whereas no significant effects on IL-10 production and hippocampal BDNF levels were observed. In addition, ibuprofen did not significantly reduce amyloid-β Overall, the findings of the present study suggest that some, but not all, of the adverse effects of systemic inflammation are alleviated by ibuprofen treatment.

Sections du résumé

BACKGROUND BACKGROUND
Extensive data point to the immune system as an important factor underlying the pathogenesis of brain diseases. Epidemiological studies have shown that long-term treatment with non-steroidal anti-inflammatory drugs (NSAIDs) significantly reduces the onset and progression of Alzheimer's disease. The present study aimed to investigate whether ibuprofen (IBU) is able to prevent the long-lasting alterations of brain function induced by systemic inflammation.
METHODS METHODS
Mice received intraperitoneal injections of lipopolysaccharide (LPS; 250 µg/kg/day) for seven consecutive days. Ibuprofen administration (40 mg/kg/day) was started three days before the LPS injections and continued until the last day of LPS injection. Within the next 2 weeks, mice performances on the behavioral tests were evaluated, and then brain tissue samples for biochemical analyses were collected.
RESULTS RESULTS
The findings showed that ibuprofen significantly improved mice's performance in the passive avoidance test and reduced anxiety- and depressive-like behaviors. However, ibuprofen could not significantly improve spatial memory in the Morris water maze test and recognition ability in the novel object recognition test. TNF-α and IL-1β cytokines levels and malondialdehyde (MDA) concentration in the hippocampal tissues of LPS-treated mice were significantly lowered by ibuprofen treatment, whereas no significant effects on IL-10 production and hippocampal BDNF levels were observed. In addition, ibuprofen did not significantly reduce amyloid-β
CONCLUSION CONCLUSIONS
Overall, the findings of the present study suggest that some, but not all, of the adverse effects of systemic inflammation are alleviated by ibuprofen treatment.

Identifiants

pubmed: 32696348
doi: 10.1007/s43440-020-00141-y
pii: 10.1007/s43440-020-00141-y
doi:

Substances chimiques

Amyloid beta-Peptides 0
Anti-Inflammatory Agents, Non-Steroidal 0
Cytokines 0
Lipopolysaccharides 0
Peptide Fragments 0
amyloid beta-protein (1-40) 0
Malondialdehyde 4Y8F71G49Q
Ibuprofen WK2XYI10QM

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

130-142

Subventions

Organisme : National Institute for Medical Research Development
ID : 982737

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Auteurs

Hossein Salmani (H)

Student Research Committee, Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

Mahmoud Hosseini (M)

Division of Neurocognitive Sciences, Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. HosseiniM@mums.ac.ir.
Neuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. HosseiniM@mums.ac.ir.
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran. HosseiniM@mums.ac.ir.

Yousef Baghcheghi (Y)

Student Research Committee, Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.

Zahra Samadi-Noshahr (Z)

Student Research Committee, Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Physiology, School of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.

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