HE Jiancheng, WANG Wenwu. Effect of Tianma Gouteng Yin on Apoptosis of Dopaminergic Neurons in Parkinson’s Disease Model Rats[J]. Journal of Traditional Chinese Medicine2010, 51(11): 1024-1027.
HE Jiancheng, WANG Wenwu. Effect of Tianma Gouteng Yin on Apoptosis of Dopaminergic Neurons in Parkinson’s Disease Model Rats[J]. Journal of Traditional Chinese Medicine2010, 51(11): 1024-1027.DOI: 10.13288/j.11-2166/r.2010.11.036.
Objective To study the effect of Tianma Gouteng Yin (Decoction of Gastrodia and Uncaria) on apoptosis of dopaminergic neurons in Parkinson’s disease (PD) model rats.Methods The PD models were established by injecting 6-hydroxy dopamine into the right substantia nigra of brain and treated with Tianma Gouteng Yin (5.13g/ml) for 14 days. At the same time the normal control group and pseudo-operation group were set up for comparison. The changes of dopaminergic nerons apoptosis were observed with the help of TUNEL and transmission electron microscopy and the expression of substantia nigra Bcl-2 and Bax was observed with immunohistochemical method.Results The positive TUNEL stained nucleus could be detected on the samples in the model group and the apoptosis cells were significantly more than those of the normal control group and pseudo-operation group (P<0.01). In the Tianma Gouteng Yin group
there was also apoptotic nucleus found
but the apoptotic cells were much less than in the model group (P<0.01). Compared with the normal control group and pseudo-operation group
the expression of Bax and Bcl-2
especially Bax
in the model group was significantly higher. Compared with the model group
the expression of Bcl-2 in the Tianma Gouteng Yin group was significantly higher
but that of Bax was significantly lower (P<0.01). The electron microscopy examination showed that the pathological changes of neurons in Tianma Gouteng Yin group were significantly milder than those in the model group.Conclusion Tianma Gouteng Yin restrains significantly the apoptosis of dopaminergic neurons in rats with Parkinson’s disease and its mechanism may be actualized by lifting the expression of Bcl-2 and restraining the activation of Bax through anti-oxidation stress.