Introduction: Motor-function modulation through Pyridine-3-carboxylic acid was assessed against. Haloperidol induced Parkinson’s disease (PD) in albino-mice. The objectives of this study were to test the effect of Haloperidol in development of PD, effectiveness of Pyridine-3-carboxylic acid in mice and evaluation of the motor-function changes in mice before and after treatment.
Methods: The study was divided into 3 phases: During Phase-I (randomization), all the subjects were randomly divided into 4 groups and trained for wire-hanging, grip strength, vertical rod and swim tests for 1 week. During Phase-II (disease induction), PD was induced by intra-peritoneal (ip) administration of Haloperidol (HP) in a dose of 1 mg/kg/d for 7 days. Group-A comprised of healthy controls, Group-B (Diseased), Group-C (HP+Pyridine-3-carboxylic acid 7.15 mg/kg/d) and Group-D (HP+Pyridine-3-carboxylic acid15 mg/kg/d).
Results: Pyridine-3-carboxylic acid treatment continued for 5 weeks. During Phase-III the above mention tests were performed and the effects of Pyridine-3-carboxylic acid were recorded. However, in swim test Group D is statistically insignificant as compared to Group B (p=0.284). In recent study, haloperidol is found to be effective in inducing motor function anomalies likewise in Parkinson’s disease including movement slowness, difficulties with gait and balance.
Conclusion: oral administration of Pyridine-3-carboxylic acid improved Motor-function changes in diseased mice. Therefore, it is concluded that Pyridine-3-carboxylic acid may help to alleviate PD symptoms.
Introduction: The objectives of current study are to test for Neuroprotective activity of Camellia sinensis in rat model of stroke and to evaluate the effect of Camellia Sinensis as anti-thrombolytic agent and in lowering the impact of disease with the behavioural changes before and after the induction of Stroke. Methods: Forty male albino rats were subjected to middle cerebral artery occlusion method for induction of stroke. Camellia sinensis extract was administered orally for 21 consecutive days prophylactically. Ischaemic rats administered the same volume of tap water were used as a control group. Functional outcome tests (Pasta, forelimb flexion, cylinder, staircase) were performed. Rats were subjected to surgical procedures after 21 days' treatment for analysis of stroke recovery. Results: Treatment with Camellia sinensis extract of 400 mg/kg PO significantly (P=0.000) enhanced neurological recovery in all tests performed. There was no significant difference of infarct volume among the experimental groups treated with Camellia sinensis extract 200 mg/kg PO. Conclusion: The outcomes of this study was vivid that Camellia sinensis extract is safe and effective mediator in clot dissolution and stroke reversal in rat model. It is the first agent found effective in no behavioural modification or adverse effects using its extract. Therefore, there is a need to evaluate, assess and appraise its desired characteristics and therapeutics in human subjects.
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