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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 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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The present study investigated the possible effect of BMMS in protecting against memory impairment in an Alzheimer's disease model induced by scopolamine in mice. Another objective was to evaluate the involvement of oxidative stress and Na/K ATPase activity in cerebral cortex and hippocampus of mice. Male Swiss mice were divided into four groups: groups I and III received canola oil (10 ml/kg, intragastrically (i.g.)), while groups II and IV received BMMS (10 mg/kg, i.g.). Thirty minutes after treatments, groups III and IV received scopolamine (1 mg/kg, intraperitoneal (i.p.)), while groups I and II received saline (5 ml/kg, i.p.). Behavioral tests were performed thirty minutes after scopolamine or saline injection. Cerebral cortex and hippocampus were removed to determine the thiobarbituric acid reactive species (TBARS) levels, non-protein thiols (NPSH) content, catalase (CAT) and Na/K ATPase activities. The results showed that BMMS pretreatment protected against the reduction in alternation and latency time induced by scopolamine in the Y-maze test and step-down inhibitory avoidance, respectively. In the Barnes maze, the latency to find the escape box and the number of holes visited were attenuated by BMMS. Locomotor and exploratory activities were similar in all groups. BMMS pretreatment protected against the increase in the TBARS levels, NPSH content and CAT activity, as well as the inhibition on the Na/K ATPase activity caused by scopolamine in the cerebral cortex. In the hippocampus, no significant difference was observed. In conclusion, the present study revealed that BMMS protected against the impairment of retrieval of short-term and long-term memories caused by scopolamine in mice. Moreover, antioxidant effect and protection on the Na/K ATPase activity are involved in the effect of compound against memory impairment in AD model induced by scopolamine.

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Available online xxxKeywords: Inflammation Pleurisy Nanoparticles Cytokines Meloxicam a b s t r a c t The development of new treatments for inflammation continues to be of high interest, since long-acting effect is critical for patients. We investigated whether meloxicam-loaded lipid-core nanocapsules (M-NC) have an anti-inflammatory action superior to a free drug (M-F) on a mouse pleurisy model, by analyzing the time-course of leukocytes migration in the pleural fluid. Male adult Swiss mice were divided into six groups for each time (24; 48and 72 h) and were pretreated with blank nanocapsules (17 ml/kg) or M-NC (5 mg/kg) or free meloxicam (M-F) (5 mg/kg). After pretreatments, mice received saline (0.9%) or carrageenan (Cg) (1%) into pleural cavity. Four hours after Cg or saline administration, animals were killed, pleural cavity was washed and pleural fluid was collected for the determination of total leukocytes. Cytokines levels, differential leukocyte count and a-1-acid glycoprotein (AGP) levels were determined only at 48 h of pretreatment, which had effect on total leukocyte count. M-NC were effective against the increase in total and differential leukocyte counts and pleural exudate caused by Cg, while M-F had no effect. M-NC had superior