Objective: To explore the neuroprotective effects of electroacupuncture (EA) on hypoxic-ischemic encephalopathy (HIE) and to further investigate the role of glial cell line-derived neurotrophic factor (GDNF) fa...Objective: To explore the neuroprotective effects of electroacupuncture (EA) on hypoxic-ischemic encephalopathy (HIE) and to further investigate the role of glial cell line-derived neurotrophic factor (GDNF) family receptor member RET (rearranged during transfection) and its key downstream phosphatidylinositol 3 kinase (PI-3K)/protein kinase B (Akt) pathway in the process. Methods: A total of 220 seven-day-old SD rats (of either sex, from 22 broods) were randomly divided into two groups, one (30 rats) for sham-surgery group and the other (190 rats) for HIE model group. The HIE model was established using the left common carotid artery ligation method in combination with hypoxic treatment. The successfully established rats were randomly divided into five groups, including control model group, EA group, sham-EA group, antagonist group and antagonist plus electroacupuncture group, with 35 rats in each group. Baihui (GV 20), Dazhui (GV 14), Quchi (LI 11) and Yongquan (KI 1) acupoints were chosen for acupuncture. EA was performed at Baihui and Quchi for 10 min once a day for continuous 1, 3, 7 and 21 days, respectively. The rats were then killed after the operation and injured cerebral cortex was taken for the measurement of neurologic damage by hematoxylin-eosin (HE) staining and the degenerative changes of cortical ultrastructure by transmission electron microscopy. RET mRNA level and Akt protein level were detected by real-time reverse-transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively. Results: EA could ameliorate neurologic damage of the first somatic sensory area (SITr) and alleviate the degenerative changes of ultrastructure of cortical neurons in rats subjected to HIE. And the longer acupuncture treatment lasted, the better its therapeutic effect would be. This was accompanied by gradually increased expression of GDNF family receptor RET at the mRNA level and its downstream signaling Akt at the protein l展开更多
基金Supported by the 45th China Postdoctoral Science Foundation(No.20090450856)
文摘Objective: To explore the neuroprotective effects of electroacupuncture (EA) on hypoxic-ischemic encephalopathy (HIE) and to further investigate the role of glial cell line-derived neurotrophic factor (GDNF) family receptor member RET (rearranged during transfection) and its key downstream phosphatidylinositol 3 kinase (PI-3K)/protein kinase B (Akt) pathway in the process. Methods: A total of 220 seven-day-old SD rats (of either sex, from 22 broods) were randomly divided into two groups, one (30 rats) for sham-surgery group and the other (190 rats) for HIE model group. The HIE model was established using the left common carotid artery ligation method in combination with hypoxic treatment. The successfully established rats were randomly divided into five groups, including control model group, EA group, sham-EA group, antagonist group and antagonist plus electroacupuncture group, with 35 rats in each group. Baihui (GV 20), Dazhui (GV 14), Quchi (LI 11) and Yongquan (KI 1) acupoints were chosen for acupuncture. EA was performed at Baihui and Quchi for 10 min once a day for continuous 1, 3, 7 and 21 days, respectively. The rats were then killed after the operation and injured cerebral cortex was taken for the measurement of neurologic damage by hematoxylin-eosin (HE) staining and the degenerative changes of cortical ultrastructure by transmission electron microscopy. RET mRNA level and Akt protein level were detected by real-time reverse-transcription polymerase chain reaction (RT-PCR) and western blot analysis, respectively. Results: EA could ameliorate neurologic damage of the first somatic sensory area (SITr) and alleviate the degenerative changes of ultrastructure of cortical neurons in rats subjected to HIE. And the longer acupuncture treatment lasted, the better its therapeutic effect would be. This was accompanied by gradually increased expression of GDNF family receptor RET at the mRNA level and its downstream signaling Akt at the protein l
文摘目的:观察针刺对脑缺血大鼠不同时间段神经元凋亡及STAT5表达的调节作用,探讨脑缺血后针刺调节机体自稳态的可能作用机制。方法:SD大鼠造模成功后随机分为假手术组、模型组、针刺组、AG490组和AG490+针刺组,再分为2 h、1 d、3 d、7 d及21 d 5个亚组,与假手术组对照。电凝闭右大脑中动脉复制脑缺血模型,针刺大椎、百会干预。采用透射电镜观察神经元超微结构,TUNEL观测神经元凋亡,原位杂交技术检测STAT5 m RNA含量。结果:透射电镜观察和TUNEL检测细胞凋亡发展趋势相似,在缺血3 d后大鼠神经元凋亡达到高峰。针刺组抗细胞凋亡均优于同时段的其他组别,AG490+针刺组有一定改善作用,模型组和AG490组神经元凋亡明显。脑缺血后2 h^1 d模型组和针刺组STAT5 m RNA升高,AG490+针刺组低于针刺组(P<0.01)。3~7 d针刺组高于模型组(P<0.05),AG490组和AG490+针刺组的含量较低(均P<0.01)。结论:针刺能改善脑缺血细胞凋亡,调节机体自稳态的内在机制可能是通过上调STAT5的水平而实现的。