OBJECTIVE: To observe the influence of electroacupuncture (EA) therapy on the expression of tyrosine hydroxylase (TH) and cyclooxygenase-2 (COX-2) proteins of Substantia Nigra cells(SNc) in the rotenone-induced Parkinson's disease(PD) rats, so as to explore the mechanism of EA underlying improvement of PD. METHODS: Forty rats were randomly divided into normal, sham-operation (sham), model and EA groups (n = 10/group). The PD model was established by successive subcutaneous injection of rotenone (highly selective lesions of nigrostriatal dopaminergic neurons) for 28 days. EA (2 Hz, 1 mA) was applied to bilateral "Fengfu" (GV 16) and "Taichong" (LR 3) for 20 min, once daily for 14 days. The expression levels of TH and COX-2 proteins in the Substantia Nigra of midbrain were detected with Western blotting. RESULTS: Compared with the normal group, the expression level of TH protein in the model group was significantly decreased (P < 0.01), and that of COX-2 protein in the model group was significantly increased (P < 0.01). After the EA treatment, the expression level of TH in the EA group was obviously upregulated (P < 0.01), and that of COX-2 protein in the EA group was considerably down-regulated (P < 0.01). No significant differences were found between the normal and sham groups in the expression levels of TH and COX-2 proteins (P > 0.05). CONCLUSION: EA therapy can decrease inflammation mediator COX-2 protein expression and upregulate TH protein expression in the Substantia Nigra of midbrain in PD rats, which may contribute to its effect in relieving PD in clinic.
OBJECTIVE: To observe the influence of electroacupuncture (EA) therapy on the expression of tyrosine hydroxylase (TH) and cyclooxygenase-2 (COX-2) proteins of Substantia Nigra cells(SNc) in the rotenone-induced Parkinson's disease(PD) rats, so as to explore the mechanism of EA underlying improvement of PD. METHODS: Forty rats were randomly divided into normal, sham-operation (sham), model and EA groups (n = 10/group). The PD model was established by successive subcutaneous injection of rotenone (highly selective lesions of nigrostriatal dopaminergic neurons) for 28 days. EA (2 Hz, 1 mA) was applied to bilateral "Fengfu" (GV 16) and "Taichong" (LR 3) for 20 min, once daily for 14 days. The expression levels of TH and COX-2 proteins in the Substantia Nigra of midbrain were detected with Western blotting. RESULTS: Compared with the normal group, the expression level of TH protein in the model group was significantly decreased (P < 0.01), and that of COX-2 protein in the model group was significantly increased (P < 0.01). After the EA treatment, the expression level of TH in the EA group was obviously upregulated (P < 0.01), and that of COX-2 protein in the EA group was considerably down-regulated (P < 0.01). No significant differences were found between the normal and sham groups in the expression levels of TH and COX-2 proteins (P > 0.05). CONCLUSION: EA therapy can decrease inflammation mediator COX-2 protein expression and upregulate TH protein expression in the Substantia Nigra of midbrain in PDrats, which may contribute to its effect in relieving PD in clinic.