Angiotensin-converting enzymes are increasingly being tested in therapeutics of Parkinsonism. The objective of the present study was to evaluate the behavioral changes and neuroprotective role of captopril in the rotenone model of Parkinsonism in rats. Adult Wistar albino rats were divided into four groups of six each. Parkinsonism was induced with rotenone (3 mg/Kg intraperitoneal) in three groups. The experimental group was treated with captopril (20 mg/kg intraperitoneal). The effects were compared with a standard group treated with levodopa (12 mg/Kg) and Benserazide (3 mg/Kg). Behavioral effects were evaluated by the rotarod test, spontaneous locomotor activity, hole board test, forced swim test, and tail suspension test. Neuroprotection was noted with an estimation of glutathione and lipid peroxidation from rat brain homogenate. Levels of dopamine, serotonin, and GABA were also noted. Haematoxylin and eosin-stained sections of the brain evaluated for any histoarchitectural changes. Rats pre-treated with captopril have shown a significant increase in the duration of stay in the rotarod test, a significant increase in the number of head dipping in hole board test, significant lower duration of immobility in forced swim test and tail suspension test. Captopril has a significant neuroprotective role, as evidenced by a significant decrease in levels of glutathione and a significant increase in lipid peroxidase, myeloperoxidase, catalase, superoxide dismutase, and MAO-B levels. Captopril has significant effects on brain neurotransmitters, as evidenced by dopamine, serotonin, and acetylcholine. Captopril has shown significant neuronal protection by increased expression of Bcl-2 immunohistochemistry in rotenone-induced PD. Captopril has shown significant improvement in motor coordination (as evidenced through rotarod test), exploratory behavior (hole board test), depression (forced swimming test, and tail suspension test). Captopril significantly reduces oxidative stress conditions. Captopril has not shown major histoanatomical changes in the rotenone model. Angiotensin-converting enzyme inhibitors; neuroprotection; dopaminergic neurons; Parkinsonism; rotenone model

Non-motor symptoms such as depression, dementia, autonomic nervous system problems may be more evident in the later part of Parkinsonism. L-dopa is largely ineffective for non-motor symptoms. The objective of the present study was to evaluate the anti-depressant and neuroprotective role of captopril and perindopril in paraquat mice model of Parkinsonism. Adult Swiss albino mice were divided into five groups of six each. Parkinsonism was induced with paraquat (7mg/kg bodyweight at an interval of 2 days) in four groups. Experimental group was treated with captopril (20mg/kg intraperitoneal) and perindopril (5mg/kg intraperitoneal). Depression influences on behaviour was studied with forced swim test and tail suspension test. Oxidative stress markers – glutathione, lipid peroxidation assay, myeloperoxidase activity, catalase, superoxide dismutase, monoamine oxidase A and B are carried out in one hemisection of the mice brain to evaluate the neuroprotective role of the test drugs. The test group mice exposed to captopril and perindopril had significantly less immobility time in both forced swim test and tail suspension test in comparison to the paraquat group, indicating anti-depressant effects of these drugs. Lipid peroxidation, myeloperoxidase activity, catalase, superoxide dismutase, monoamine oxidase B levels were significantly increased in both captopril and perindopril groups in comparison to the control group. Captopril and perindopril have shown beneficial effects for depression (as evidenced through forced swimming test and tail suspension test) in paraquat model of Parkinsonism. These drugs reduce the oxidative stress in paraquat mice model of Parkinsonism

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