[The alterations of apoptosis factor Bcl-2/Bax in the early Parkinson's disease rats and the protective effect of scorpion venom derived activity peptide].
[The alterations of apoptosis factor Bcl-2/Bax in the early Parkinson's disease rats and the protective effect of scorpion venom derived activity peptide].
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Original abstract
OBJECTIVE: To explore the alterations of apoptosis factor Bcl-2/Bax in the early Parkinson's disease (PD) rats and the protective effect of scorpion venom derived bioactive peptide. METHODS: Healthy male SD rats (180-220 g) were randomly divided into 4 groups (n = 10): early PD model group, sham operation group, scorpion venom derived bioactive peptide control group, scorpion venom derived bioactive peptide therapy group. 6-hydroxydopamine (6-OHDA) was used to prepare the early PD rat model. The immunohistochemistry was used to detect the expression of Bax and Bcl-2 and further explore the mechanism of anti-apoptosis regarding the neuroprotective effect of scorpion venom derived bioactive peptide. RESULTS: The results indicated that compared with the control rats, the immunostaining of Bax in the brain increased significantly while that of Bcl-2 decreased significantly in the lesion side of 6-OHDA treated rats. Interestingly, scorpion venom derived bioactive peptide could attenuate the above abnormal changes. CONCLUSION: Up-regulation of Bax and down-regulation of Bcl-2 could participate in the early stage of PD and the anti-apoptotic mechanism could be involved in the neuroprotective effect exerted by scorpion venom derived activity peptide regarding the dopaminergic neuron in the early stage.