Piracetam improves cognitive function in animals and in human beings, but its mechanism of action is still not completely known. In the present study, we investigated whether enzymes involved in extracellular adenine nucleotide metabolism, adenosine triphosphate diphosphohydrolase (NTPDase), 5'-nucleotidase and adenosine deaminase (ADA) are affected by piracetam in the hippocampus and cerebral cortex of animals subjected to scopolamine-induced memory impairment. Piracetam (0.02 μmol/5 μL, intracerebroventricular, 60 min pre-training) prevented memory impairment induced by scopolamine (1 mg/kg, intraperitoneal, immediately post-training) in the inhibitory avoidance learning and in the object recognition task. Scopolamine reduced the activity of NTPDase in hippocampus (53 % for ATP and 53 % for ADP hydrolysis) and cerebral cortex (28 % for ATP hydrolysis). Scopolamine also decreased the activity of 5'-nucleotidase (43 %) and ADA (91 %) in hippocampus. The same effect was observed in the cerebral cortex for 5'-nucleotidase (38 %) and ADA (68 %) activities. Piracetam fully prevented scopolamine-induced memory impairment and decrease of NTPDase, 5'-nucleotidase and adenosine deaminase activities in synaptosomes from cerebral cortex and hippocampus. In vitro experiments show that piracetam and scopolamine did not alter enzymatic activity in cerebral cortex synaptosomes. Moreover, piracetam prevented scopolamine-induced increase of TBARS levels in hippocampus and cerebral cortex. These results suggest that piracetam-induced improvement of memory is associated with protection against oxidative stress and maintenance of NTPDase, 5'-nucleotidase and ADA activities, and suggest the purinergic system as a putative target of piracetam.
Desonide is a topical corticoid used in the treatment of skin diseases and is marketed in different pharmaceutical dosage forms. Recently, the poor photostability of a commercially available hair solution after direct exposure to UVA light was verified. In this study, we investigated the ability of the antioxidants ascorbic acid, butylhydroxyanisole (BHA), butylhydroxytoluene (BHT), α-tocopherol, and the UV filter benzophenone-3 (BP-3) to prevent the photodegradation of desonide in hair solution (desonide 0.1%) and the stability of the proposed formulation under environmental conditions. The tested antioxidants were not able to prevent the photolysis of desonide, whereas the addition of 0.3% BP-3 enhanced the photostability of the drug. After 15 h of direct exposure to UVA radiation, the desonide remaining content in the hair solution with BP-3 was approximately 98%. Higher photostability was also verified under UVC radiation. Additionally, the results indicated that the formulation was stable under accelerated and room temperature conditions for 70 days, corresponding to the total period of the study.
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