摘要
目的:观察电针干预对失神经肌萎缩大鼠腓肠肌中叉头蛋白转录因子3A(fork-head protein,FOXO3A)、肌萎缩F-box蛋白(muscle atrophy F-box,MAFbx)和成肌分化抗原(myogenic differentiation antigen,Myod1)蛋白及基因表达的影响,探讨电针延缓大鼠失神经肌萎缩的可能机制。方法:雄性Sprague-Dawley大鼠随机分为假手术组、模型组及电针组,每组6只。采用钳夹坐骨神经法制备大鼠失神经腓肠肌萎缩模型。电针组选取大鼠术侧"足三里""环跳"穴进行治疗,每日1次,每次10min,连续干预14d后取材。计算各组大鼠腓肠肌湿重比,HE染色测定大鼠术侧腓肠肌纤维截面积和直径,Western blot检测大鼠术侧腓肠肌中FOXO3A、MAFbx、Myod1蛋白的相对表达量,实时荧光定量PCR检测大鼠术侧腓肠肌中FOXO3A、MAFbx及Myod1mRNA的相对表达量。结果:与假手术组相比,模型组大鼠腓肠肌湿重比、肌纤维截面积和直径均显著下降(P<0.01),电针组高于模型组(P<0.01)。与假手术组相比,模型组大鼠腓肠肌中FOXO3A、MAFbx、Myod1蛋白及mRNA表达量显著升高(P<0.01);与模型组相比,电针干预后FOXO3A、MAFbx蛋白及mRNA表达量显著降低(P<0.01),Myod1蛋白及mRNA表达量显著升高(P<0.01)。结论:电针可能通过抑制FOXO3A、MAFbx的表达同时上调Myod1的表达,影响骨骼肌蛋白水解的速率和肌卫星细胞分化的水平,在延缓失神经肌萎缩的同时促进肌萎缩修复。
Objective To observe the effect of electroacupuncture(EA)on morphological changes of denervated gastrocnemius(GS)and the expression of fork-head protein(FOXO3 A),muscle atrophy F-box(MAFbx)and myogenic differentiation antigen(Myod1)in sciatic nerve injury rats,so as to reveal its mechanism underlying improvement of myoatrophy.Methods Eighteen male Sprague-Dawley rats were randomly divided into sham operation,model and EA groups(n=6 per group).The model of gastrocnemius atrophy was established by crushing the right sciatic nerve.Then,EA(2 Hz)was applied to the right'Zusanli'(ST36)and'Huantiao'(GB30)for 10 min,once a day for 14 successive days.The wet weight of the GS on both sides was weighted to calculate the wet weight ratio(the injured side/the healthy side),and the cross-sectional area(CSA)and diameter of GS fibers were measured after H.E.staining.The expressions of FOXO3 A,MAFbx and Myod1 protein and mRNA in the GS tissue were tested using Western blot and fluorescence quantitative PCR,separately.Results Following modeling,the GS wet weight ratio,CSA and fiber diameter were smaller in the model group than those in the sham group(P<0.01),and were significantly higher in the EA group than in the model group(P<0.01).H.E.staining showed that the GS fibers became smaller and the myocyte got round in the model group,while the GS fibers were bigger and the myocyte was relatively regular in morphology in the EA group.After modeling,the expression levels of FOXO3 A,MAFbx and Myod1 mRNA and protein were evidently higher in the model group(P<0.01);Moreover,after EA treatment,modeling-induced increasing of expression levels of FOXO3 Aand MAFbx mRNA and protein were revised(P<0.01),while the increased expression level of Myod1 was further up-regulated relavant to that in the model group(P<0.01).Conclusion EA of ST36 and GB30 can suppress the up-regulated expression of FOXO3 Aand MAFbx mRNA and protein and further promote the expression of Myod1 mRNA and protein in the GS tissue in rats with denervated GS atrophy,which may
作者
吴梦佳
唐成林
黄思琴
赵丹丹
罗翱
张安宁
安荟羽
谭程方
邱丽
WU Meng-jia;TANG Cheng-lin;HUANG Si-qin;ZHAO Dan-dan;LUO Ao;ZHANG An-ning;AN Huiyu;TAN Cheng-fang;QIU Li(College of Traditional Chinese Medicine,Chongqing Medical University,Chongqing400016,China;Chongqing Key Laboratory of Traditional Chinese Medicine for Prevention and Treatment of Metabolic Diseases,Chongqing Medical University,Chongqing400016,China)
出处
《针刺研究》
CAS
CSCD
北大核心
2019年第4期253-257,275,共6页
Acupuncture Research
基金
国家自然科学基金项目(No.81273870)
