电针对椎动脉型颈椎病家兔的治疗作用机制  

Therapeutic Mechanism of Electroacupuncture on Cervical Spondylosis of Vertebral Artery Type in Rabbits

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作  者:刘芳[1] 顾逸文 方浩亮 杨雨烨 LIU Fang;GU Yiwen;FANG Haoliang;YANG Yuye(Department of Acupuncture and Moxibustion,Zhejiang Hospital of Integrated Traditional Chinese and Western Medicine,Hangzhou 310003,China;The Second Clinical Medical College of Zhejiang Chinese Medical University,Hangzhou 310053,China)

机构地区:[1]浙江省中西医结合医院针灸科,杭州310003 [2]浙江中医药大学第二临床医学院,杭州310053

出  处:《世界中医药》2025年第3期399-403,410,共6页World Chinese Medicine

基  金:国家自然科学基金项目(81704144);浙江省中医药科技计划项目(2020ZB190);国家中医药管理局第五批全国中医临床优秀人才研修项目(国中医药人教函〔2022〕1号);浙江省卫生高层次人才培养工程项目(浙卫办〔2020〕18号)。

摘  要:目的:探讨电针通过兔磷酸肌醇3激酶(PI3K)/蛋白激酶B(AKT)/哺乳动物雷帕霉素靶蛋白(mTOR)对椎动脉型颈椎病(CSA)家兔的治疗作用。方法:将50只实验兔按随机数字表法分为正常对照组、模型对照组、电针组、磷酸肌醇3激酶抑制剂组、电针+磷酸肌醇3激酶抑制剂组,每组10只。对模型对照组、电针组、磷酸肌醇3激酶抑制剂组和电针+磷酸肌醇3激酶抑制剂组实验兔进行CSA模型制备。电针+磷酸肌醇3激酶抑制剂组、磷酸肌醇3激酶抑制剂组注射PI3K抑制剂Wortmannin(浓度24μg/kg);正常对照组与模型对照组仅给予相同固定;电针组和电针+磷酸肌醇3激酶抑制剂组给予电针“风池穴”,每天1次,连续治疗14 d。观察各组行为学变化,酶联免疫吸附试验(ELISA)法检测实验兔椎动脉PI3K、p-AKT、mTOR、低氧诱导因子(HIF-1α)、血管内皮生长因子(VEGF)水平。结果:正常对照组实验兔无明显行为学变化;模型对照组实验兔精神萎靡、缩肩拱背、食欲减退、活动减少;电针组、电针+磷酸肌醇3激酶抑制剂组实验兔精神萎靡、活动减少、缩肩拱背改善。与正常对照组比较,模型对照组、磷酸肌醇3激酶抑制剂组、电针+磷酸肌醇3激酶抑制剂组实验兔椎动脉PI3K、p-AKT、mTOR水平低(均P<0.01);与模型对照组比较,电针组实验兔椎动脉PI3K、p-AKT、mTOR水平高(均P<0.05);模型对照组、磷酸肌醇3激酶抑制剂组、电针+磷酸肌醇3激酶抑制剂组实验兔椎动脉PI3K、p-AKT、mTOR水平比较差异均无统计学意义(均P>0.05);与磷酸肌醇3激酶抑制剂组比较,电针+磷酸肌醇3激酶抑制剂组实验兔椎动脉PI3K、p-AKT、mTOR水平高(均P<0.05)。与正常对照组比较,模型对照组、磷酸肌醇3激酶抑制剂组实验兔椎动脉HIF-1α、VEGF水平低(均P<0.05);电针组、电针+磷酸肌醇3激酶抑制剂组实验兔椎动脉HIF-1α、VEGF水平与正常对照组比较差异均无统计学意义(均PObjective:To investigate the therapeutic effects of electroacupuncture(EA)on vertebral artery-type cervical spondylosis(CSA)in rabbits via the phosphoinositide 3-kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR)pathway.Methods:Fifty experimental rabbits were randomly divided into five groups(n=10 per group):normal control,model control,EA,PI3K inhibitor,and EA+PI3K inhibitor groups.The CSA model was established in all groups except the normal control group.Rabbits in the PI3K inhibitor and EA+PI3K inhibitor groups were injected with the PI3K inhibitor wortmannin(24μg/kg).The normal and model control groups were subjected to the same fixation without treatment.The EA and EA+PI3K inhibitor groups received EA stimulation at Fengchi(GB20)once daily for 14 days.Behavioral changes were observed,and enzyme-linked immunosorbent assay(ELISA)was used to detect PI3K,p-AKT,mTOR,hypoxia-inducible factor 1-alpha(HIF-1α),and vascular endothelial growth factor(VEGF)levels in the vertebral artery.Results:Rabbits in the normal control group exhibited no significant behavioral abnormalities,while those in the model control group showed lethargy,hunched posture,reduced appetite,and decreased activity.EA and EA+PI3K inhibitor groups showed improvements in lethargy,reduced activity,and hunched posture.Compared with the normal control group,PI3K,p-AKT,and mTOR levels in the vertebral artery were significantly lower in the model control,PI3K inhibitor,and EA+PI3K inhibitor groups(all P<0.01).Compared with the model control group,PI3K,p-AKT,and mTOR levels were significantly higher in the EA group(all P<0.05).No significant differences in PI3K,p-AKT,and mTOR levels were observed among the model control,PI3K inhibitor,and EA+PI3K inhibitor groups(all P>0.05).Compared with the PI3K inhibitor group,the EA+PI3K inhibitor group showed significantly higher PI3K,p-AKT,and mTOR levels(all P<0.05).HIF-1αand VEGF levels in the vertebral artery were significantly lower in the model control and PI3K inhibitor groups than in t

关 键 词:椎动脉型颈椎病 电针 磷酸肌醇3激酶 蛋白激酶B 哺乳动物雷帕霉素靶蛋白 低氧诱导因子 血管内皮生长因子  

分 类 号:R246[医药卫生—针灸推拿学]

 

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