Li Ke, He Hong, Hu Mao-Qing, Zhang Lin
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2016 Jul;36(7):875-878.
To explore the mechanism of electropuncture (EA) for reducing diet-induced obesity (DIO) rat weight through tuberous sclerosis complex 1 (TSC1 )-mammalian target of rapa- mycin (mTOR) signal pathway in hypothalamus.
Forty male SD rats were randomly divided into the model group (n =30) and the normal control group (n =10). DIO rat model was prepared by high fat forage for 12 successive weeks. Successfully modeled 19 rats were further randomly divided into the model group (n =9) and the EA group (n =10). EA at Tianshu (ST25) , Sanyinjiao (SP6) , Zhongwan ( RN12) , Zusanli (ST36) was performed in the EA group, 5 successive days per week with a 2-day rest, 4 weeks in total. No intervention was given to rats in the model group and the normal control group. Body weight was observed in all rats. Methylation of TSC1 promotor was detected by bisulfite sequencing method. mRNA expression of mTOR in hypothalamus was detected by RT-PCR.
After EA treatment body weight in the EA group were obviously reduced (P <0. 05). Compared with the normal control group, body weight was not statistically different between the model group and the EA group after treatment (P> 0. 05). Methylation rate of TSC1 promotor was higher in model group (94. 0% ±4. 5%) than in the normal control group (87. 0% ±3. 6%) and the EA group (87. 4% ±3. 9%) (P <0. 05). Expression of mTOR in the model group (1. 84 ±0. 51) was higher than that in the normal control group (1. 02 ±0. 22) and the EA group (1. 46 ±0. 29) (P <0. 05).
EA could lower DIO rats' body weight by down-regulating methylation rate of TSC1 promotor and regulating expression of mTOR in hypothalamus.
探讨电针通过下丘脑结节性硬化复合物1（TSC1）-雷帕霉素哺乳动物靶蛋白（mTOR）信号通路减轻饮食诱导肥胖（DIO）大鼠体重的机制。
40只雄性SD大鼠随机分为模型组（n = 30）和正常对照组（n = 10）。连续12周给予高脂饲料制备DIO大鼠模型。将成功造模的19只大鼠进一步随机分为模型组（n = 9）和电针组（n = 10）。电针组取天枢（ST25）、三阴交（SP6）、中脘（RN12）、足三里（ST36）进行电针治疗，每周连续治疗5天，休息2天，共治疗4周。模型组和正常对照组大鼠不给予干预。观察所有大鼠的体重。采用亚硫酸氢盐测序法检测TSC1启动子的甲基化情况。采用RT-PCR法检测下丘脑mTOR的mRNA表达。
电针治疗后电针组大鼠体重明显降低（P < 0.05）。与正常对照组比较，治疗后模型组与电针组大鼠体重差异无统计学意义（P > 0.05）。模型组TSC1启动子甲基化率（94.0%±4.5%）高于正常对照组（87.0%±3.6%）和电针组（87.4%±3.9%）（P < 0.05）。模型组mTOR表达（1.84±0.51）高于正常对照组（1.02±0.22）和电针组（1.46±0.29）（P < 0.05）。
电针可通过下调TSC1启动子甲基化率及调节下丘脑mTOR表达降低DIO大鼠体重。
