世界中医药

作者	单位
刘芳1，顾逸文2，方浩亮2，杨雨烨2	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

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中文摘要:

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24 μg/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P>0.05）；与模型对照组比较，正常对照组实验兔椎动脉HIF-1α、VEGF水平高（均P<0.05）；电针组、磷酸肌醇3激酶抑制剂组、电针+磷酸肌醇3激酶抑制剂组实验兔椎动脉HIF-1α、VEGF水平与模型对照组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HIF-1α、VEGF水平高（均P<0.05）。结论：电针可通过激活PI3K/AKT/mTOR信号通路治疗CSA模型兔。

English Summary:

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(24 μg/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-1α and VEGF levels in the vertebral artery were significantly lower in the model control and PI3K inhibitor groups than in the normal control group(both P<0.05).However，no significant differences were observed in HIF-1α and VEGF levels between the EA and EA+PI3K inhibitor groups and the normal control group(both P>0.05).Compared with the model control group，the normal control group exhibited significantly higher HIF-1α and VEGF levels(both P<0.05).No significant differences were found in HIF-1α and VEGF levels between the model control group and the EA，PI3K inhibitor，or EA+PI3K inhibitor groups(all P>0.05).Compared with the PI3K inhibitor group，the EA+PI3K inhibitor group had significantly higher HIF-1α and VEGF levels(both P<0.05).Conclusion:EA may exert therapeutic effects on CSA model rabbits by activating the PI3K/AKT/mTOR signaling pathway.

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