furostanol-i and Disease-Models--Animal

Parkinson's disease (PD) is the most widespread motor-affecting disease affecting majorly middle- and late age population. Thus, in the current study, we intended to explore the neuroprotective effect of protodioscin (Proto) against 6-hydroxydopamine (6-OHDA)-induced PD rat model.. After induction of PD with the injection of 6-OHDA, the different dose of Proto was administered for the duration of experimental protocol (2 months). We have scrutinized the consequence of Proto on the cognitive behaviours via Moris water maze (MWM), and recognition of novel objects and its location tasks. The effect of Proto was also investigated on the expression of Nrf2 in human neuroblastoma SHSY5Y cells via western blot analysis.. The results showed significant decrease in travelled distance as compared by the lesion treated group. Further significant difference was revealed in the latency time to detect the platform that is visible and it confirmed that, there were no noteworthy dissimilarity was observed in the visual and motor function ability. The result also suggests that, the activation of Nrf2 is the possible mechanism of neuroprotection of Proto against PD.. As a concluding remark, the present study confirmed the neuroprotective role of Proto against PD both in in vitro and in vivo models.

Topics: Animals; Behavior, Animal; Brain; Cell Line, Tumor; Cognition; Dihydroxyphenylalanine; Diosgenin; Disease Models, Animal; Dose-Response Relationship, Drug; Exploratory Behavior; Humans; Male; Maze Learning; Neuroprotective Agents; NF-E2-Related Factor 2; Parkinsonian Disorders; Rats, Wistar; Saponins

Epilepsy is associated with increased morbidity and mortality together and places a large financial burden on individuals and society. To evaluate the anticonvulsant action of protodioscin (PDSN) in experiments with animals with pilocarpine-induced convulsions. We assessed the activity of PDSN in pilocarpine induced seizures in combination with different agents which are acting via diverse receptors, such as atropine, memantine, nimodipine, diazepam, and flumazenil, to determine the exact receptors responsible for the action of PDSN. Furthermore, the level of antioxidant markers was investigated in the cerebellum and cerebral cortex in mice to define the antioxidant action of PDSN. The effects of PDSN on proapoptotic markers (i.e., Bcl-2, Bax, and caspase-3) was investigated via western blot analysis. PDSN significantly enhanced latency to the first convulsion and survival compared to the group treated with pilocarpine alone. Moreover, PDSN improved animal survival, and subjects experiencing no convulsions. Striatal glutamate and aspartate levels were not modified, and gamma amino butyric acid (GABA) levels increased, as a result of treatment with PDSN. The results suggest that the anticonvulsive action of PDSN is dependent on inhibitory amino acids. PDSN treatment also significantly decreased nitrite levels in the blood and brain cortex compared to the normal control. In the western blot analysis, PDSN exerted its neuroprotective effect via the upregulation of Bcl-2 and downregulation of Bax and caspase-3. The results of this study suggest that PDSN exerts neuroprotective effects via multiple mechanisms.

Topics: Animals; Anticonvulsants; Apoptosis; bcl-2-Associated X Protein; Behavior, Animal; Biomarkers; Caspase 3; Corpus Striatum; Diosgenin; Disease Models, Animal; Down-Regulation; Epilepsy; gamma-Aminobutyric Acid; Humans; Male; Mice; Pilocarpine; Proto-Oncogene Proteins c-bcl-2; Saponins; Up-Regulation