电针干预JNK通路调控2型糖尿病大鼠骨骼肌IRS-1磷酸化的机制研究  

Mechanism Study on EA Regulating Skeletal Muscle IRS-1 Phosphorylation Through JNK Signaling Pathway in Type 2 Diabetic Rats

作　　者：杨灿 曹昺焱[1] 张广德[1] YANG Can;CAO Bingyan;ZHANG Guangde(Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing 100091,China)

机构地区：[1]中国中医科学院西苑医院,北京100091

出　　处：《针灸临床杂志》2022年第7期60-64,共5页Journal of Clinical Acupuncture and Moxibustion

基　　金：国家自然科学基金青年项目,编号:81704192;中央级公益性科研院所基本科研业务费专项资金资助,编号ZZ13-YQ-013。

摘　　要：目的:观察低频电针对2型糖尿病大鼠血糖和胰岛素抵抗的干预作用,并从调控骨骼肌胰岛素受体底物1(IRS-1)磷酸化的角度,对电针的干预效果进行解释。方法:以Purina#5008饲料喂养ZDF大鼠制备2型糖尿病动物模型,并以ZL大鼠为空白组。成模动物根据空腹血糖随机分为模型组和电针组。电针组以15 Hz、2 mA的连续波电针“后三里”“三阴交”“脾俞”“胃脘下俞”穴组,留针20 min,每日1次,6次/周,6周进行干预;空白组及模型组不干预。于全部干预结束后检测大鼠空腹血糖、空腹胰岛素含量,计算胰岛素抵抗指数(HOMA-IR),判断电针对2型糖尿病大鼠胰岛素抵抗的干预作用;取大鼠骨骼肌以Western blot法检测磷酸化氨基末端激酶(p-JNK)水平及p-IRS-1 Ser307含量,探讨电针干预效果的机理。结果:低频电针可显著降低模型动物激增的空腹血糖和胰岛素抵抗指数,显著下调模型动物骨骼肌p-JNK thr183/tyr185磷酸化及p-IRS-1 Ser307蛋白表达。结论:低频电针可显著改善2型糖尿病大鼠高血糖及胰岛素抵抗状态,上述作用可能通过下调骨骼肌JNK活性、抑制骨骼肌IRS-1丝氨酸磷酸化实现。Objective:To observe the effect of low frequency electro-acupuncture(EA)on fasting blood glucose(FBG)and insulin resistance(IR)in type 2 diabetic rats,and to explain the intervention mechanism of EA in terms of regulating phosphorylation of skeletal muscle insulin receptor substrate-1(IRS-1).Methods:Type 2 diabetic model rats were prepared by induction feeding of Purina#5008 rodent chow on Zucker diabetic fatty(ZDF)rats.And Zucker lean(ZL)rats were taken as the blank control.The successful modeling rats were randomly divided into the model group and the EA group according to fasting blood glucose.The EA group was intervened by electro-needling Housanli(ST36),Sanyinjiao(SP6),Pishu(BL20),and Weiwanxiashu(EX-B3)with 15 Hz and 2 mA electric wave,once per day,6 times per week for 6 weeks.No intervention was applied to the rats in the blank control group and the model group.FBG and insulin concentration were measured to calculate HOMA-IR,which reflects EA’s effects on IR.The phosphorylation level of phospho-C-Jun N-terminal kinase(p-JNK)and the content of p-IRS-1 Ser307 in skeletal muscle were measured by Western blot.Results:Low frequency EA could significantly decrease the dramatic increase of FBG and IR in type 2 diabetic rats,and remarkably down-regulated the phosphorylation of skeletal muscle p-JNK thr183/tyr185 and the protein expression of p-IRS-1 Ser307.Conclusion:Low frequency EA can regulate IR of type 2 diabetic rats,which mechanism may be related to down-regulating skeletal muscle JNK activity and inhibiting IRS-1 serine phosphorylation.

关 键 词：电针 2型糖尿病 C-JUN氨基末端激酶 胰岛素受体底物1 

分 类 号：R246.1[医药卫生—针灸推拿学]