Journal
METABOLIC BRAIN DISEASE
Volume 31, Issue 4, Pages 793-802Publisher
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s11011-016-9812-3
Keywords
Nanoparticles; Meloxicam; Amyloid-beta; Drug-delivery; Cyclooxygenase
Categories
Funding
- FAPERGS [1924-2551/13-1]
- CAPES
- UNIFRA
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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 beta-peptide (a beta) 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 a beta (3 nmol/ 3 mu l/ per site, intracerebroventricular) or vehicle (3 mu l/ 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. a beta 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 a beta, and Na+, K+-ATPase is involved in the effect of M-NC.
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