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电针对急性心肌缺血大鼠海马谷氨酸系统的影响OA北大核心CSTPCD

Effects of Electroacupuncture on the Hippocampus Glutamate System of Acute Myocardial Ischemia Rats

中文摘要英文摘要

目的 观察电针对急性心肌缺血(AMI)大鼠海马谷氨酸(Glu)、代谢型谷氨酸受体 2/3(mGluR2/3)和凋亡相关蛋白表达的影响,探讨电针抗AMI的作用机制.方法 50只SD大鼠随机分为假手术组、模型组、电针组和抑制剂组,每组10只.除假手术组外,其余各组采用左冠状动脉前降支结扎法建立AMI大鼠模型.电针组于双侧"神门""通里"予电针刺激,30 min/次,1次/d,连续3 d;抑制剂组于造模后30 min经侧脑室注入mGluR2/3抑制剂LY341459.HE染色观察心肌组织形态,ELISA检测心肌组织胱天蛋白酶-3(Caspase-3)活性和海马组织Glu含量,免疫荧光染色检测海马组织mGluR2/3表达,TUNEL染色检测海马组织细胞凋亡情况,Western blot检测海马组织磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B(Akt)和Caspase-3蛋白表达.结果 与假手术组比较,模型组大鼠心肌细胞稀疏、肿胀,炎性细胞浸润严重;心肌组织Caspase-3活性显著升高,海马组织Glu含量、mGluR2/3阳性表达及凋亡细胞数均显著增加(P<0.01),海马组织PI3K、Akt蛋白表达显著降低,Caspase-3蛋白表达显著升高(P<0.01);与模型组比较,电针组和抑制剂大鼠心肌细胞水肿减轻,炎性细胞浸润减少,心肌组织Caspase-3活性显著降低,海马组织Glu含量、mGluR2/3阳性表达及凋亡细胞数均显著减少(P<0.01),海马组织PI3K、Akt蛋白表达显著升高,Caspase-3蛋白表达显著降低(P<0.01).结论 电针可改善AMI大鼠心肌损伤,其机制可能与激活PI3K/Akt信号通路,进而抑制海马组织mGluR2/3过度表达、减少Glu蓄积、抑制海马神经细胞凋亡,减轻神经毒性有关.

Objective To observe the effects of electroacupuncture(EA)on glutamate(Glu),metabotropic glutamate receptor 2/3(mGluR2/3)and apoptosis related proteins expression in hippocampus in rats with acute myocardial ischemia(AMI);To explore the mechanism of EA against AMI.Methods Totally 50 SD rats were randomly divided into sham-operation group,model group,EA group and inhibitor group,with 10 rats in each group.Except for the sham-operation group,the rats were treated with ligation at the left anterior descending coronary artery to establish AMI model.The rats in the EA group was treated with EA at"Shenmen"and"Tongli",30 minutes each time,once a day for 3 consecutive days.The rats in the inhibitor group were treated with injection of LY341459 via the lateral ventricle 30 min after modeling.HE staining was used to observe myocardial tissue morphology,and ELISA was used to detect Caspase-3 activity in myocardial tissue and Glu content in hippocampal tissue,immunofluorescence staining was used to detect mGluR2/3 expression in hippocampal tissue,TUNEL staining was used to detect apoptosis in hippocampal tissue cells,Western blot was used to detect the expressions of PI3K,Akt,and Caspase-3 protein in hippocampal tissue.Results Compared with the sham-operation group,the myocardial cells of the model group rats showed sparse and swelling with severe infiltration of inflammatory cells;the activity of Caspase-3 in myocardial tissue significantly increased,and the Glu content,positive expression of mGluR2/3,number of apoptotic cells in hippocampal tissue significantly increased(P<0.01),and the expressions of PI3K and Akt proteins in hippocampal tissue were significantly decreased,while the expression of Caspase-3 protein significantly increased(P<0.01).Compared with the model group,myocardial cell edema and inflammatory cell infiltration were reduced in the EA group and inhibitor group,the activity of Caspase-3 in myocardial tissue was significantly decreased,the Glu content,positive expression of mGluR2/3,and number of apoptotic cells in hippocampal tissue were significantly reduced(P<0.01),the expressions of PI3K and Akt proteins in hippocampal tissue significantly increased,while the expression of Caspase-3 protein significantly decreased(P<0.01).Conclusion EA can improve myocardial injury in AMI rats,and its mechanism may be related to activation of PI3K/Akt signaling pathway,inhibition of hippocampal mGluR2/3 overexpression,reduction of Glu accumulation,inhibition of apoptosis of hippocampal neurons and reduction of neurotoxicity.

童思佳;王堃;吴生兵;周美启

安徽中医药大学研究生院,安徽 合肥 230038安徽中医药大学新安医学教育部重点实验室,安徽 合肥 230038安徽中医药大学针灸经络研究所,安徽 合肥 230038安徽中医药大学针灸经络研究所,安徽 合肥 230038||安徽省中医药科学院亳州中医药研究所,安徽 亳州 236800

中医学

急性心肌缺血电针海马谷氨酸代谢型谷氨酸受体2/3大鼠

acute myocardial ischemiaelectroacupuncturehippocampusGlumetabotropic glutamate receptors 2/3rats

《中国中医药信息杂志》 2024 (003)

基于谷氨酸能神经元调控海马-HPA轴探讨针刺抗心肌缺血的作用机制

92-97 / 6

国家自然科学基金(82004462);安徽省中医药领军人才建设项目(2019年);浙江中医药大学科研开放基金(ZYXYB2019002)

10.19879/j.cnki.1005-5304.202306008

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