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Effects of erythropoietin on the expression of tumor necrosis factor-alpha and Bax after facial nerve axotomy in rats 被引量:6
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作者 Wei Zhang Shengyu Lue Ziying Yu Ming Bi Bin Sun 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第6期444-449,共6页
This study sought to evaluate the effect of high-dose erythropoietin (EPO; 5 000 IU/kg) on the expression of tumor necrosis factor-alpha (TNF-α) and Bax in the facial nucleus after facial nerve transection in rat... This study sought to evaluate the effect of high-dose erythropoietin (EPO; 5 000 IU/kg) on the expression of tumor necrosis factor-alpha (TNF-α) and Bax in the facial nucleus after facial nerve transection in rats. A total of 42 Wistar rats of both genders were used in this study, and 40 rats were randomly divided into 2 groups: EPO group and model group. The EPO group was treated with EPO once a day for 5 days at a dose of 5 000 IU/kg body weight. The model group was treated with saline of the same amount. At day 3 after EPO (or saline) treatment, the right facial nerves of the 40 rats were transected at the level of the stylomastoid foramen, with the left sides untreated. The remaining 2 rats that did not undergo axotomy served as the control group. The surviving motor neurons in operated rats were counted in coronal paraffin sections of the facial nucleus. The expression of TNF-a and Bax in the facial nucleus was detected by immunohistochemical staining at days 3, 7, 14, 21, and 28 after axotomy. At days 14, 21, and 28 after facial nerve axotomy, a significantly greater proportion of facial motor neurons survived in the EPO group than in the model group. After axotomy, the expression of TNF-a and Bax increased in motor neurons in both the EPO and the model groups. TNF-o expression reached its peak level at day 14 after axotomy, while Bax expression reached its peak level at day 21. TNF-α expression was much lower in the EPO group than in the model group at all time points. No significant difference in Bax expression was found between the EPO and the model groups. These results indicate that high-dose EPO treatment attenuates the increase in TNF-α expression in the facial nucleus and reduces the loss of motor neurons after facial nerve transection in rats. However, high-dose EPO treatment has little effect on Bax expression. 展开更多
关键词 ERYTHROPOIETIN tumor necrosis factor-a Bcl-2-associated X protein facial motor neuron
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Plastic Changes of Synapses and Excitatory Neurotransmitter Receptors in Facial Nucleus Following Facial-facial Anastomosis
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作者 陈沛 宋俊 +1 位作者 罗凌惠 龚树生 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2008年第6期714-718,共5页
The remodeling process of synapses and neurotransmitter receptors of facial nucleus were observed. Models were set up by facial-facial anastomosis in rat. At post-surgery day (PSD) 0,7,21and 60, synaptophysin (p38... The remodeling process of synapses and neurotransmitter receptors of facial nucleus were observed. Models were set up by facial-facial anastomosis in rat. At post-surgery day (PSD) 0,7,21and 60, synaptophysin (p38), NMDA receptor subunit 2A and AMPA receptor subunit 2 (GluR2) were observed by immunohistochemical method and semi-quantitative RT-PCR, respectively. Mean-while, the synaptic structure of the facial motorneurons was observed under a transmission electron microscope (TEM). The intensity of p38 immunoreactivity was decreased, reaching the lowest value at PSD day 7, and then increased slightly at PSD 21. Ultrastructurally, the number of synapses in nucleus of the operational side decreased, which was consistent with the change in P38 immunoreactivity. NMDAR2A mRNA was down-regulated significantly in facial nucleus after the operation (P〈0.05), whereas AMPAR2 mRNA levels remained unchanged (P〉0.05). The synapses innervation and the expression of NMDAR2A and AMPAR2 mRNA in facial nucleus might be modified to suit for the new motor tasks following facial-facial anastomosis, and influenced facial nerve regeneration and recovery. 展开更多
关键词 facial motor neurons SYNAPSE neurotransmitter receptor EXCITABILITY control
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