Larissa Finger Schaffer

Gallic acid decreases vacuous chewing movements induced by reserpine in rats

Involuntary oral movements are present in several diseases and pharmacological conditions; however, their etiology and efficient treatments remain unclear. Gallic acid is a natural polyphenolic acid found in gall nuts, sumac, oak bark, tea leaves, grapes and wine, with potent antioxidant and antiapoptotic activity. Thus, the present study investigated the effects of gallic acid on vacuous chewing movements (VCMs) in an animal model induced by reserpine. Rats received either vehicle or reserpine (1mg/kg/day, s.c.) during three days, followed by treatment with water or different doses of gallic acid (4.5, 13.5 or 40.5mg/kg/day, p.o.) for three more days. As result, reserpine increased the number of VCMs in rats, and this effect was maintained for at least three days after its withdrawal. Gallic acid at two different doses (13.5 and 40.5mg/kg/day) has reduced VCMs in rats previously treated with reserpine. Furthermore, we investigated oxidative stress parameters (DCFH-DA oxidation, TBARS and thiol levels) and Na(+),K(+)-ATPase activity in striatum and cerebral cortex, however, no changes were observed. These findings show that gallic acid may have promissory use in the treatment of involuntary oral movements.

Harpagophytum procumbens Prevents Oxidative Stress and Loss of Cell Viability In Vitro

Harpagophytum procumbens, popularly known as devil’s claw, is a plant commonly used in the treatment of diseases of inflammatory origin. The anti-inflammatory effects of H. procumbens have been studied; however, the mechanism of action is not elucidated. It is known that excess of reactive oxygen and nitrogen species may contribute to increasing tissue damage due to inflammation. In the present study, we examined the effects of H. procumbens infusion, crude extract and fractions on lipid peroxidation (brain homogenates) induced by different pro-oxidants (Fe2+ or sodium nitroprusside) and the effects of ethyl acetate fraction (rich in phenolic compounds) on antioxidant defenses (catalase activity and thiol levels) and cell damage (brain cortical slices) induced by different pro-oxidants. All tested extracts of H. procumbens inhibited lipid peroxidation in a concentration-dependent manner. Furthermore, the ethyl acetate fraction had the highest antioxidant effects either by decreasing lipid peroxidation and cellular damage or restoring thiols levels and catalase activity. Taken together, our results showed that H. procumbens acts either by preventing oxidative stress or loss of cell viability. Thus, the previously reported anti-inflammatory effect of H. procumbens could also be attributed to its antioxidant activity.

Gabapentin prevents behavioral changes on the amphetamine-induced animal model of schizophrenia

Fig. 1. Effect of gabapentin on behavioral changes induced by acute amphetamine administratio for 5min in an open field arena, analyses of workingmemory in Ymaze by (B) percentage of cor 15 min (animals tested in pairs) and (D) stereotyped behavior of mice observed in glass cage absence (0) or presence and amount (from 1 to 3) types of abnormal movements (head nodd way ANOVA followed by post hoc Tukeys test. Data are expressed as mean ± S.E.M. for 11–1 control group, p b 0.05 when compared with the amphetamine group.

Gabapentin reduces haloperidol-induced vacuous chewing movements in mice

ABSTRACT Tardive dyskinesia (TD) is a common adverse effect observed in patients with long‐term use of typical antipsychotic medications. A vacuous chewing movement (VCM) model induced by haloperidol has been used to study these abnormalities in experimental animals. The cause of TD and its treatment remain unknown, but several lines of evidence suggest that dopamine receptor supersensitivity and gamma‐aminobutyric acid (GABA) insufficiency play important roles in the development of TD. This study investigated the effects of treatment with the GABA‐mimetic drug gabapentin on the development of haloperidol‐induced VCMs. Male mice received vehicle, haloperidol (1.5 mg/kg), or gabapentin (GBP, 100 mg/kg) intraperitoneally during 28 consecutive days. Quantification of VCMs was performed before treatment (baseline) and on day 28, and an open‐field test was also conducted on the 28th day of treatment. The administration of gabapentin prevented the manifestation of haloperidol‐induced VCMs. Treatment with haloperidol alone reduced the locomotor activity in the open‐field test that was prevented by co‐treatment with gabapentin. We did not find any differences among the groups nor in the tyrosine hydroxylase (TH) or glutamic acid decarboxylase (GAD) immunoreactivity or monoamine levels in the striatum of mice. These results suggest that treatment with gabapentin, an analog of GABA, can attenuate the VCMs induced by acute haloperidol treatment in mice without alterations in monoamine levels, TH, or GAD67 immunoreactivity in the striatum. HighlightsGabapentin prevented haloperidol‐induced vacuous chewing movements.Gabapentin attenuates the reduction in locomotor activity caused by haloperidol.Any alteration was found in TH, GAD67 or monoamines levels in striatum of mice treated with haloperidol and/or gabapentin.

Sporothrix brasiliensis produces the highest levels of oxidative stress in a murine model among the species of the Sporothrix schenckii complex

INTRODUCTION: We compared indicators of oxidative stress in the tissue of mice infected with strains from Sporothrix schenckii complex. METHODS: Mice were inoculated with Sporothrix brasiliensis, Sporothrix schenckii sensu stricto, Sporothrix globosa, Sporothrix mexicana or Sporothrix albicans. The activity of catalase and glutathione were accessed in the liver and spleen. RESULTS: Animals infected with S. brasiliensis exhibited splenomegaly and significant decrease in catalase activity, and protein and non-protein thiol content compared to animals infected with the other species. CONCLUSIONS: Sporothrix brasiliensis exhibits higher pathogenicity compared to other species of the Sporothrix schenckii complex by increasing oxidative stress in animal tissue.