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安徽中医学院针灸经络研究所
纸质出版日期:2006
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吴子建, 汪克明, 王月兰, 等. 电针对心肌缺血细胞G蛋白信号通路的影响[J]. 针刺研究, 2006,(5):264-267.
WU Zi-jian, WANG Ke-ming, WANG Yue-lan, et al. Effect of Electroacupuncture on Signal Transduction of G-protein in Rat Ischemic Myocardial Cells[J]. Acupuncture research, 2006, (5): 264-267.
目的:分析电针对缺血心肌细胞G蛋白信号通路的影响
揭示电针抗心肌缺血的分子作用途径。方法:健康SD雄性大鼠20只
随机分为正常组、模型组、电针正常“神门”组、电针模型“神门”组
每组5只。采用冠状动脉结扎法复制心肌缺血模型
然后电针“神门”穴
予以1.3 mA、2 Hz方波刺激
每日1次
3 d后动物麻醉状态下活体取材
用基因芯片技术筛选各组G蛋白及其相关基因。结果:筛选到表达G蛋白15个
通过cAMP或Ca2+途径影响下游基因表达
调节细胞转录和应答。电针“神门”特异性G蛋白2个
主要是G蛋白γ亚型通过cAMP影响下游蛋白激酶Aβ2调节细胞转录。结论:电针抗心肌缺血可以通过调节多种G蛋白影响缺血心肌细胞内的基因表达
从而发挥保护心肌的作用
以Gi和Gq最为重要;心经与心脏间具有相对特异的分子联系途径
可能主要是Gγ和PKAβ2途径。
Objective: To analyze the effect of electroacupuncture(EA) on myocardial cellular signal transduction of G-protein in myocardial ischemia(MI) rats so as to explore the molecular pathway of EA against MI injury. Methods: Twenty male SD rats were randomized into normal
model
EA-normal and EA-model groups
5 rats in each group.MI model was established by occlusion of the descending anterior branch of the left coronary artery under anesthesia with 10% chloral hydrate(0.36 mL/100 g).EA (1.3 mA
2 Hz
300 μs in the duration of pulse) was applied to "Shenmen"(HT 7) for 20 min
once daily continuously for 3 days.Three days later
the myocardial tissue sample was taken for shifting out related G-proteins and corresponding genes by using gene chip technology. Results: In comparison with model group
after EA of "Shenmen"(HT 7)
782 differentially expressed genes were found
of which
328 were upregulated and 454 downgrelated;compared with normal group
426 differentially expressed genes were found in EA-normal group
among them
217 genes were upregulated and the other 209 downregulated in the expression.Further analysis showed that
21 genes were associated with G-protein signal transduction pathway
15 genes(L01115.1
Gng11
Adcy2
Calm3
Ppp3ca
Adcy5
Gnao
Prkcc
Arhgef1
RGD:619921
Pccb
Prkcd
Ppp3cb
Gng5
Gnai1) had an apparent expression in the 4 groups
4 genes(Gnaz
Prkcb1
Adcy3 and Adcy8) had no marked changes
and the rest 2(Gng8 and Prkar2b) were differentially expressed genes.Of the 2 differentially expressed genes
Gng8 displayed weaker and stronger expression in EA-normal and EA-model groups respectively
and had no expression in normal and model groups
suggesting being closely related to EA-HT 7;while Prkar2b showed no expression in normal and EA-normal groups
and had a detectable expression in model and EA-model groups
suggesting being related to MI. Conclusion: EA-HT 7 can affect gene expression of ischemic myocardiocytes;among the differentially expressed genes being closely associated with G-protein signaling pathway
Gng8 and Prkar2b may play an important role in EA-induced protective action on myocardial ischemia.
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