Neuroprotective and Antioxidant Effects of Riparin I in a Model of Depression Induced by Corticosterone in Female Mice.

BACKGROUND: Depression is a common, chronic, and often recurrent serious mood disorder. Conventional antidepressants present limitations that stimulate the search for new drugs. Antioxidant and neuroprotective substances are potential antidepressant agents. In this context, riparin I (RIP I) has presented promising results, emerging as a potential source of a new therapeutic drug. In this study, the antidepressant effect of RIP I was evaluated in an animal model of depression induced by corticosterone (CORT). The involvement of neuroprotective and antioxidant mechanisms in the generation of this effect was also assessed. METHODS: Female mice were submitted to CORT for 21 days and treated with RIP I in the last 7 days. Behavioral and neurochemical analyses were performed. RESULTS: The administration of RIP I reversed the depressive and psychotic-like behavior, as well as the cognitive impairment caused by CORT, in addition to regulating oxidative stress parameters and BDNF levels in depression-related brain areas. CONCLUSION: These findings suggest that RIP I can be a strong candidate for drugs in the treatment of depression.

Antinociceptive activity of Riparin II from Aniba riparia: Further elucidation of the possible mechanisms.

Riparin II (RipII) has an anti-inflammatory activity potentially due its ability to decrease TNF-α and IL-1ß production and its histamine antagonism. The objective of this study was to evaluate the role of RipII in the pain process and the possible antinociceptive mechanisms involved, using classic models of nociception. Male Swiss mice were used in the assays. Determinate the acute toxicity according to the OECD 425 test guideline. The models used were the acetic acid-, formalin-, hot plate and glutamate-induced nociception. For evaluation of antinociceptive effect, the involvement of TRPV1, TRPA1, TRPM8, ASICS, Bradykinin, PKC and PKA were performed using the paw licking using agonists. The acute toxicity study did not detect any clinical signs or changes in behavior or mortality. RipII, administered orally (25 and 50 mg/kg) caused a reduction of nociception induced by acetic acid, formalin (on the second phase) and glutamate. In the investigation of antinociceptive mechanism, we used capsaicin (2.2 µg/paw), cinnamaldehyde (10 nmol/paw), menthol (1.2 µmol/paw), ASICS (2% acetic acid, pH 1.98) and bradykinin (10 µg/paw). The results showed that TRPV1, TRPA1, TRPM8, ASICS and bradykinin play a role in the antinociceptive effect of RipII. The results also showed that PKA is involved too. These data demonstrate that RipII has a low or not toxicity and produced an important antinociceptive effect through mechanisms that probably involve an interaction, at least in part, TRPV1, TRPA1, TRPM8, ASICS, bradykinin and PKA participate in the RipII's antinociceptive effect.