深刺“环跳”在大鼠坐骨神经损伤修复中的抗凋亡机制  

Anti-apoptotic Mechanism of Deep Electroacupuncture at“Huantiao”(GB 30)in Repair of the Injured Sciatic Nerve in Rats

作　　者：闫泓池 马铁明[3] 陶星[1,4] 马贤德 YAN Hong-chi;MA Tie-ming;TAO Xing;MA Xian-dea(Graduate School;College of Acupuncture-moxibustion and Message;Teaching Experimental Center,Liaoning University of Traditional Chinese Medicine,Shenyang 110847,China;Northeast International Hospital,Shenyang 110847;Wuhan Municipal Hospital of Traditional Chinese Medicine,Wu han 430000)

机构地区：[1]辽宁中医药大学研究生院,沈阳110847 [2]东北国际医院,沈阳110847 [3]辽宁中医药大学针灸推拿学院,沈阳110847 [4]武汉市中医院,武汉430000 [5]辽宁中医药大学教学实验中心,沈阳110847

出　　处：《针刺研究》2018年第11期711-717,共7页Acupuncture Research

基　　金：国家自然科学基金项目(No.81574051);辽宁省高等学校创新团队项目(No.LT 2015016)

摘　　要：目的:从细胞凋亡角度探讨深刺"环跳"对坐骨神经损伤修复的作用机制。方法:SD大鼠随机分为空白组、模型组、深刺组、浅刺组,每组12只。采用硅胶管挤压法复制大鼠坐骨神经慢性损伤模型。两个针刺组在高频小动物超声仪引导下针刺"环跳"穴,深刺组在高频超声引导下观察针尖触及神经干引发的神经冲动,浅刺组针尖刺入肌肉层下约3～5mm,未触及神经干,不引发神经冲动,两组均连接电针仪治疗,每日1次,连续治疗14d。检测大鼠坐骨神经功能指数(SFI)和运动神经传导速度(MNCV),苏木素伊红(HE)染色法观察坐骨神经病理形态的改变,TUNEL法检测细胞凋亡情况,免疫组化法检测大鼠L 4—L 5背根神经节中磷脂酰肌醇-3羟基激酶(PI 3K)、蛋白激酶B(AKT)的表达情况。结果:模型组SFI、MNCV均低于空白组(P<0.01,P<0.05),坐骨神经损伤后神经细胞凋亡数以及L 4—L 5背根神经节中PI 3K、AKT的表达高于空白组(P<0.05)。与模型组比较,深刺组及浅刺组SFI、MNCV明显升高(P<0.01,P<0.05),坐骨神经损伤后神经细胞凋亡数明显降低(P<0.05),L 4—L 5背根神经节中PI 3K、AKT的表达明显升高(P<0.05);且深刺组各项指标的变化较浅刺组更显著(P<0.01,P<0.05)。结论:深刺"环跳"穴可以通过激活PI 3K-AKT信号通路,抑制大鼠坐骨神经损伤后的神经细胞凋亡,促进神经损伤修复。Objective To observe the effect of deep electroacupuncture（EA）at＂Huantiao＂（GB 30）on functional and pathological changes of the damaged sciatic nerve and apoptosis-related factors in lumbar dorsal root ganglia（DRGs）in rats,so as to study its mechanisms underlying relieving sciatica.Methods Forty-eight SD rats were randomly divided into normal,model,deep EA（DEA）and shallow EA（SEA）groups（n=12 in each group）.The sciatic nerve injury model was established by silicone tube extrusion of the sciatic nerve stem.For DEA group,acupuncture needles were inserted into GB 30 about 8 mm deep to induce nerve impulse under the guidance of high-frequency ultrasound,and the needles were inserted into GB 30 about 3—5 mm in the SEA group.The EA treatment was applied to bilateral GB 30 for 20 min beginning from the 15 th day on after modeling,once daily for 14 days.The sciatic nerve function index（SFI）and motor nerve conduction velocity（MNCV）were recorded and calculated.Pathological changes of the sciatic nerve were displayed by H.E.staining.The cell apoptosis and expression of PI 3 Kand AKT proteins in lumbar 4—5 DRGs were detected by TUNEL staining,and immunohistochemistry,respectively.Results In comparison with the normal group,the SFI and MNCV were significantly decreased（P〈0.01,P〈0.05）,the number of neuronal apoptosis and the expression of PI 3 Kand AKT in L 4—L 5 DRGs were significantly increased in the model group（P〈0.05）.Following the treatment,the SFI,MNCV,and the number of neuronal apoptosis were reversed compared with the model group（P〈0.01,P〈0.05）,both PI 3 Kand AKT expression levels were significantly up-regulated in both DEA and SEA groups（P〈0.05）.The therapeutic effects were significantly better in the DEA group than in the SEA group in down-regulating cell apoptosis number and in up-regulating SFI,MNCV,and PI 3 Kand AKT protein expression on day 28 of modeling（P〈0.01,P〈0.05）.Conclusion Deep EA at GB 30 can activate PI 3 K-AKT signaling pathway

关 键 词：坐骨神经损伤 深刺 环跳穴 细胞凋亡 PI 3K-AKT 

分 类 号：R245.97[医药卫生—针灸推拿学]