首页|期刊导航|西部中医药|基于ERK通路电针大鼠内关穴对糖尿病肢体缺血再灌注心肌损伤的研究

基于ERK通路电针大鼠内关穴对糖尿病肢体缺血再灌注心肌损伤的研究OA

Study on the Effect of Electroacupuncture at the Neiguan Acupoint(PC6)in Rats on Diabetic Limb Ischemia-Reperfusion-Induced Myocardial Injury via the ERK Signaling Pathway

中文摘要英文摘要

目的:通过电针内关穴作为干预措施,观察糖尿病肢体缺血再灌注(ischemia-reperfusion,IR)动物模型血清酶学和细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)通路蛋白的表达,探讨其治疗机制.方法:将80只SD大鼠随机分为空白组、模型组、电针组及西药组.将除空白组以外的其他3组分别制备糖尿病模型和肢体IR模型,并在肢体IR模型制备前后7天分别进行相应干预.取各阶段大鼠血液及心脏组织,测定血清内肌酸激酶同工酶(creatine kinase-MB,CK-MB)、肌钙蛋白I(cardiac troponin I,cTnI)和乳酸脱氢酶(lactate dehydrogenase,LDH)值,以及心肌组织内蛋白激酶B(protein kinase B,Akt)、磷酸化蛋白激酶B(phosphorylated Akt,p-Akt)、细胞外信号调节激酶1/2(ERK1/2)、磷酸化细胞外信号调节激酶1/2(phosphorylated ERK1/2,p-ERK1/2)的蛋白表达水平.结果:肢体IR造模后,相较于空白组,其他3组血清内CK-MB、cTnI、LDH值均升高(P<0.05);相较于模型组,电针组和西药组血清内心肌酶谱值显著降低(P<0.05).继续干预7天后,相较于模型组,电针组和西药组血清内cTnI、LDH值显著降低(P<0.05),但西药组血清内CK-MB值与模型组相比差异无统计学意义(P>0.05).肢体IR造模后,电针组与西药组较模型组p-Akt/Akt、p-ERK/ERK比值均升高(P<0.05);电针组较空白组p-Akt/Akt比值升高(P<0.05),而西药组较空白组p-Akt/Akt比值降低(P<0.05).继续干预7天后,电针组较空白组和模型组p-Akt/Akt比值升高(P<0.05),p-ERK/ERK比值降低(P<0.05);西药组较空白组和模型组p-Akt/Akt、p-ERK/ERK比值均降低(P<0.05).结论:电针内关穴可减轻糖尿病肢体IR所致的心肌组织损伤,其作用机制可能与上调Akt和ERK信号通路的活性有关.

Objective:To investigate the effects of electroacupuncture at the Neiguan acupoint(PC6)on serum enzyme levels and the expressions of extracellular signal-regulated kinase(ERK)pathway proteins in a rat model of diabetic limb ischemia-reperfusion(IR),and to discuss its therapeutic mechanism.Methods:A total of 80 Sprague-Dawley(SD)rats were randomly divided into four groups:blank group,model group,electroacupuncture(EA)group,and Western medicine group.Diabetes models and limb ischemia-reperfusion(IR)models were established in the three groups except the blank group.Corresponding interventions were administered for seven days before and after the establishment of the limb IR model.Blood samples and cardiac tissue were collected from each group at different stages.To measure serum levels of creatine kinase-MB(CK-MB),cardiac troponin I(cTnI),and lactate dehydrogenase(LDH),and to detect the protein expression levels of protein kinase B(Akt),phosphorylated Akt(p-Akt),extracellular signal-regulated kinase 1/2(ERK1/2),and phosphorylated ERK1/2(p-ERK1/2)in myocardial tissue.Results:After limb IR modeling,compared with the blank group,the serum levels of CK-MB,cTnI,and LDH were increased in the other three groups(P<0.05).Compared with the model group,the serum myocardial enzyme levels were significantly decreased in the EA group and the Western medicine group(P<0.05).After seven days of continued intervention,compared with the model group,the serum levels of cTnI and LDH were significantly decreased in the EA group and the Western medicine group(P<0.05).However,there was no statistically significant difference in serum CK-MB level between the Western medicine group and the model group(P>0.05).After limb IR modeling,the ratios of p-Akt/Akt and p-ERK/ERK were increased in both the EA group and the Western medicine group(P<0.05),compared with the blank group,the p-Akt/Akt ratio was increased in the EA group(P<0.05),while it was decreased in the Western medicine group compared with the blank group(P<0.05).After seven days of continued intervention,compared with both the blank group and the model group,the EA group showed an increased p-Akt/Akt ratio(P<0.05)and a decreased p-ERK/ERK ratio(P<0.05).In contrast,the Western medicine group exhibited decreased ratios of both p-Akt/Akt and p-ERK/ERK compared with the blank group and the model group(P<0.05).Conclusion:Electroacupuncture at the Neiguan acupoint attenuates myocardial injury induced by diabetic limb IR,and its underlying mechanism may be associated with the upregulation of Akt and ERK signaling pathway activities.

薛阳;张杰;路潇;秦晓宇;黄伟华;丁声双;薛建军

甘肃省中医院麻醉疼痛医学中心,甘肃 兰州 730000甘肃省中医院麻醉疼痛医学中心,甘肃 兰州 730000||甘肃中医药大学,甘肃 兰州 730000甘肃中医药大学,甘肃 兰州 730000甘肃中医药大学,甘肃 兰州 730000甘肃中医药大学,甘肃 兰州 730000甘肃中医药大学,甘肃 兰州 730000甘肃省中医院麻醉疼痛医学中心,甘肃 兰州 730000

医药卫生

心肌损伤缺血再灌注电针ERK信号通路

myocardial injuryischemia-reperfusionelectroacupunctureERK signaling pathway

《西部中医药》 2026 (3)

33-37,5

甘肃省中医药管理局科研课题(GZK-2018-29).

10.12174/j.issn.2096-9600.2026.03.07

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