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Title: [Mechanism of electroacupuncture for regulation of lipid production and improvement in obesity by mediating Wnt/ β-catenin pathway through activating SIRT1].
Author: Wang YY, Liang FX, Lu W, Zhou YD, Huang XX, Yang SR.
Journal: Zhongguo Zhen Jiu; 2021 Jul 12; 41(7):774-80. PubMed ID: 34259411.
Abstract:
OBJECTIVE: To explore the mechanism of electroacupuncture (EA) for the regulation of lipid production and improvement in obesity by mediating Wnt/β-catenin pathway through activating silent information regulator 1 (SIRT1). METHODS: Of 75 Wistar male rats, 10 rats were selected randomly as the normal group and fed with standard diet. The rest rats were fed with high-fat diet for 8 weeks to establish the obesity model. Forty rats of successful modeling were randomized into a model group, an EA group, an EA plus inhibitor group (EA+I group) and an agonist group, 10 rats in each one. In the EA group, EA was applied at "Guanyuan" (CV 4), "Zhongwan" (CV 12), "Zusanli" (ST 36) and "Fenglong" (ST 40), with continuous wave, 2 Hz in frequency and around 1 mA in intensity. The needles were retained for 20 min. In the EA+I group, sirtinol solution was injected from caudal vein and EA was exerted simultaneously. In the agonist group, resveratrol solution was given by intragastric administration. The intervention of the above three groups was given once every two days, 3 times a week, consecutively for 8 weeks. Before and after intervention, body mass and Lee's index were recorded in the rats of each group. After intervention, the levels of serum total cholesterol (TC), triglyceride (TG) and free fatty acid (FFA) were detected in the rats of each group. After intervention, the mass of white adipose tissue (WAT) and the area of adipocytes were compared in the rats among the 5 groups. Using Western blot method, the protein expressions of SIRT1, glycogen synthase kinase-3β (GSK3β), β-catenin, cyclin D1 and peroxisome proliferators-activated receptor γ (PPARγ) were detected in WAT in the rats of each group. RESULTS: After intervention, compared with the model group, the body mass and Lee's index were reduced in the rats of the EA group and the agonist group (P<0.01, P<0.05), the body mass was reduced in the rats of the EA+I group (P<0.05). Compared with the normal group, the levels of serum TC, TG and FFA, as well as WAT mass were increased in the rats of the model group (P<0.01), as well as the area of adipocytes (P<0.01). Compared with the model group, the levels of serum TC and TG (except in the EA+I group), the levels of FFA and WAT mass were all decreased (P<0.01, P<0.05) and the area of adipocytes was reduced (P<0.01, P<0.05) in the EA group, the agonist group and the EA+I group. Compared with the EA group, the area of adipocytes was increased in the EA+I group (P<0.05). Compared with the normal group, the protein expressions of SIRT1, β-catenin and cyclin D1 in WAT were down-regulated (P<0.01) and the protein expressions of GSK3β and PPARγ in WAT were up-regulated (P<0.01) in the model group. Compared with the model group, the protein expressions of SIRT1, β-catenin and cyclin D1 in WAT were up-regulated (P<0.05, P<0.01) and the expressions of GSK3β and PPARγ in WAT were down-regulated (P<0.01, P<0.05) in the EA group and the agonist group, and in the EA+I group, GSK3β protein expression was down-regulated andβ-catenin protein expression was up-regulated (P<0.05). CONCLUSION: Electroacupuncture remarkably improves the body mass, Lee's index and blood lipid metabolism and reduces WAT mass and adipocyte size in obesity model rats, which is probably related to up-regulating the protein expression of SIRT1 in WAT, activating Wnt/β-catenin pathway and inhibiting the expression of PPARγ of downstream lipogenic gene so as to affect lipid production. 目的：探讨电针通过激活沉默信息调节因子1（SIRT1）介导Wnt/β-catenin通路调控脂质生成改善肥胖的机制。方法：从75只Wistar雄性大鼠中随机挑选10只为正常组，采用标准饮食喂养；剩余大鼠采用高脂饮食构建肥胖大鼠模型，共喂养8周。将造模成功的40只大鼠随机分为模型组、电针组、电针联合抑制剂组、激活剂组，每组10只。电针组电针“关元”“中脘”“足三里”“丰隆”，连续波，频率2 Hz，电流强度约1 mA，每次留针20 min；电针联合抑制剂组尾静脉注射Sirtinol溶液，并予电针同步干预；激活剂组予白藜芦醇溶液灌胃，均隔日1次，每周3次，连续干预8周。记录各组大鼠干预前后体质量、Lee's指数，检测各组大鼠干预后血清总胆固醇（TC）、三酰甘油（TG）、游离脂肪酸（FFA）水平，比较各组大鼠干预后白色脂肪组织（WAT）质量、脂肪细胞面积，并采用Western blot法检测各组大鼠干预后WAT中SIRT1、糖原合成酶激酶-3β（GSK3β）、β-连环蛋白（β-catenin）、细胞周期蛋白D1（cyclin D1）、过氧化物酶体增殖物激活受体γ（PPARγ）蛋白表达。结果：干预后，与模型组比较，电针组、激活剂组大鼠体质量减轻、Lee's指数下降（P<0.01，P<0.05），电针联合抑制剂组大鼠体质量减轻（P<0.05）。与正常组比较，模型组大鼠血清TC、TG、FFA含量及WAT质量均升高（P<0.01），脂肪细胞面积增大（P<0.01）；与模型组比较，电针组、激活剂组、电针联合抑制剂组大鼠血清TC、TG（除外电针联合抑制剂组）、FFA含量及WAT质量均降低（P<0.01，P<0.05），脂肪细胞面积减小（P<0.01，P<0.05）；与电针组比较，电针联合抑制剂组大鼠脂肪细胞面积增大（P<0.05）。与正常组比较，模型组WAT中SIRT1、β-catenin、cyclin D1蛋白表达减少（P<0.01），GSK3β、PPARγ蛋白表达增多（P<0.01）。与模型组比较，电针组和激活剂组WAT中SIRT1、β-catenin、cyclin D1蛋白表达增多（P<0.05，P<0.01），GSK3β和PPARγ蛋白表达减少（P<0.01，P<0.05）；电针联合抑制剂组GSK3β蛋白减少、β-catenin蛋白增多（P<0.05）。结论：电针可明显改善肥胖模型大鼠体质量、Lee's指数、血脂代谢，降低WAT质量以及脂肪细胞大小，其机制可能与上调WAT中SIRT1蛋白表达，激活Wnt/β-catenin信号通路，抑制下游成脂基因PPARγ的表达，从而影响脂质生成有关。.

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