ArticleMetabolic brain disease2016
Meloxicam-loaded nanocapsules as an alternative to improve memory decline in an Alzheimer's disease model in mice: involvement of Na(+), K(+)-ATPase.
Article in Metabolic brain disease, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 27 citations in OpenAlex.
- Modeling Path Importance for Effective Alzheimer's Disease Drug Repurposing.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2024Article
- Protective Effects of Inosine on Memory Consolidation in a Rat Model of Scopolamine-Induced Cognitive Impairment: Involvement of Cholinergic Signaling, Redox Status, and Ion Pump Activities.Neurochemical research · 2022Article
- Development of In Situ Gelling Meloxicam-Human Serum Albumin Nanoparticle Formulation for Nose-to-Brain Application.Pharmaceutics · 2021Article
- Successful Treatment of Pneumothorax in a Dog With Sterile Pleural Fibrosis Caused by Chylothorax.Frontiers in veterinary science · 2019Article
- A novel albumin wrapped nanosuspension of meloxicam to improve inflammation-targeting effects.International journal of nanomedicine · 2018Article
- Effects of dexamethasone and meloxicam on Borrelia burgdorferi-induced inflammation in glial and neuronal cells of the central nervous system.Journal of neuroinflammation · 2017Article
- Nerolidol-loaded nanospheres prevent behavioral impairment via ameliorating NaNaunyn-Schmiedeberg's archives of pharmacology · 2017Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to investigate the effect of meloxicam-loaded nanocapsules (M-NC) on the treatment of the memory impairment induced by amyloid β-peptide (aβ) in mice. The involvement of Na(+), K(+)-ATPase and cyclooxygenase-2 (COX-2) activities in the hippocampus and cerebral cortex was also evaluated. Mice received aβ (3 nmol/ 3 μl/ per site, intracerebroventricular) or vehicle (3 μl/ per site, i.c.v.). The next day, the animals were treated with blank nanocapsules (17 mL/kg) or M-NC (5 mg/kg) or free meloxicam (M-F) (5 mg/kg). Treatments were performed every other day, until the twelfth day. Animals were submitted to the behavioral tasks (open-field, object recognition, Y-maze and step-down inhibitory avoidance tasks) from the twelfth day. Na(+), K(+)-ATPase and COX-2 activities were performed in hippocampus and cerebral cortex. aβ caused a memory deficit, an inhibition of the hippocampal Na(+), K(+)-ATPase activity and an increase in the hippocampal COX-2 activity. M-NC were effective against all behavioral and biochemical alterations, while M-F restored only the COX-2 activity. In conclusion, M-NC were able to reverse the memory impairment induced by aβ, and Na(+), K(+)-ATPase is involved in the effect of M-NC.
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