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. 2012 Nov-Dec;44(6):774-9.
doi: 10.4103/0253-7613.103300.

Piracetam and vinpocetine ameliorate rotenone-induced Parkinsonism in rats

Affiliations

Piracetam and vinpocetine ameliorate rotenone-induced Parkinsonism in rats

Sawsan A Zaitone et al. Indian J Pharmacol. 2012 Nov-Dec.

Abstract

Objective: To evaluate the neuroprotective effect of the nootropic drugs, piracetam (PIR) and vinpocetine (VIN), in rotenone-induced Parkinsonism in rats.

Materials and methods: Sixty male rats were divided into 6 groups of 10 rats each. The groups were administered vehicle, control (rotenone, 1.5 mg/kg/48 h/6 doses, s.c.), PIR (100 and 200 mg/kg/day, p.o.) and VIN (3 and 6 mg/kg/day, p.o.). The motor performance of the rats was evaluated by the open field and pole test. Striatal dopamine level, malondialdehyde (MDA), reduced glutathione (GSH) and tumor necrosis factor-α (TNF-α) were assayed. Histopathological study of the substantia nigra was also done.

Results: Results showed that rotenone-treated rats exhibited bradykinesia and motor impairment in the open-field test. In addition, GSH level was decreased whereas MDA and TNF-α increased in striata of rotenone-treated rats as compared to vehicle-treated rats. Marked degeneration of the substantia nigra pars compacta (SNpc) neurons and depletion of striatal dopamine was also observed in the rotenone-treated rats. Treatment with PIR or VIN significantly reversed the locomotor deficits and increased striatal dopamine level. Treatment with VIN significantly (P<0.05) reduced the striatal level of MDA and GSH in comparison to rotenone group whereas TNF-α production was found to be significantly decreased in PIR group (P<0.05).

Conclusion: VIN and PIR exhibit neuroprotective activity in rotenone-induced Parkinsonism. Hence, these nootropic agents may be considered as possible candidates in the treatment of Parkinson's disease.

Keywords: Dopamine; Parkinson's disease; piracetam; rotenone; vinpocetine.

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Conflict of interest statement

Conflicting Interest: No.

Figures

Figure 1
Figure 1
Ambulation (a) and mobility duration (b) in the open field test in experimental groups. Results are expressed as mean ± SEM and analyzed using ANOVA followed by Bonferroni's post-hoc test. *P < 0.05 as compared to the vehicle group, #P < 0.05 as compared to rotenone group, ¥P < 0.05 as compared to PIR (100 mg/kg) group, P < 0.05 as compared to PIR (200 mg/kg) group. PIR: Piracetam, VIN: Vinpocetine
Figure 2
Figure 2
Time to orient downward (t-turn) (a) and total time to descend (t-total) (b) in the pole test in experimental groups. Results are expressed as mean ± SEM and analyzed using ANOVA followed by Bonferroni's post-hoc test. *P < 0.05 as compared to the vehicle group, #P < 0.05 as compared to rotenone group, ¥P < 0.05 as compared to PIR (100 mg/kg) group, P < 0.05 as compared to PIR (200 mg/kg) group. PIR: Piracetam, VIN: Vinpocetine
Figure 3
Figure 3
Striatal dopamine level in the experimental groups. Results are expressed as mean ± SEM and analyzed using ANOVA followed by Bonferroni's post-hoc test. *P < 0.05 as compared to the vehicle group, #P < 0.05 as compared to rotenone group, ¥P < 0.05 as compared to PIR (100 mg/kg) group, P < 0.05 as compared to PIR (200 mg/kg) group. PIR: Piracetam, VIN: Vinpocetine
Figure 4
Figure 4
(a) Histological changes in the brain of the experimental groups. Vehicle-treated rat shows a number of intact SNpc neurons with visible nuclei. Nigral neurons in rotenone-treated rats (1.5 mg/kg/48 h/6 doses, s.c.) show indistinct neuronal boundaries and invisible nuclei. Treatment with piracetam or vinpocetine significantly increased the number of SNpc neurons (H and E, × 240). (b) Percentage increase in the number of dopaminergic neurons in the SNpc in the experimental groups. Results are expressed as mean ± SEM. *P < 0.05 as compared to the vehicle group, #P < 0.05 as compared to rotenone group, ¥P < 0.05 as compared to PIR (100 mg/kg) group, P < 0.05 as compared to PIR (200 mg/kg) group. PIR: Piiracetam, VIN: Vinpocetine

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