Mechanisms of electroacupuncture in improving obesity-induced insulin resistance via TLR4/NF-κB inflammatory pathway in liver

LU Wei; WU Song; LI Jia; WANG Ya-yuan; ZHOU Yu-dian; LIANG Feng-xia

doi:10.13702/j.1000-0607.20210362

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Mechanisms of electroacupuncture in improving obesity-induced insulin resistance via TLR4/NF-κB inflammatory pathway in liver

更新时间：2023-08-11

- Mechanisms of electroacupuncture in improving obesity-induced insulin resistance via TLR4/NF-κB inflammatory pathway in liver
- Acupuncture Research Vol. 47, Issue 6, Pages: 504-509(2022)
- 作者机构：
  
  1. 湖北中医药大学中医临床学院
  2. 针灸治未病湖北省协同创新中心
  3. 湖北中医药大学针灸骨伤学院
- 作者简介：
- 基金信息：
- DOI：10.13702/j.1000-0607.20210362
  CLC：
- Published：2022
- 稿件说明：
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LU Wei, WU Song, LI Jia, et al. Mechanisms of electroacupuncture in improving obesity-induced insulin resistance via TLR4/NF-κB inflammatory pathway in liver[J]. Acupuncture research, 2022, 47(6): 504-509.
DOI：

LU Wei, WU Song, LI Jia, et al. Mechanisms of electroacupuncture in improving obesity-induced insulin resistance via TLR4/NF-κB inflammatory pathway in liver[J]. Acupuncture research, 2022, 47(6): 504-509. DOI： 10.13702/j.1000-0607.20210362.

摘要

目的:观察电针对胰岛素抵抗肥胖大鼠血糖、胰岛素相关指标，以及肝脏Toll样受体4(TLR4)/核转录因子κB(NF-κB)炎性反应通路的影响，探讨电针改善胰岛素抵抗肥胖的机制。方法:Wistar大鼠随机分为正常组、模型组、电针组，每组15只。采用高脂饲料喂养8周建立胰岛素抵抗肥胖大鼠模型。电针组电针“中脘”“关元”“足三里”及“丰隆”

每次10 min

每周3次，共治疗8周。分别在干预前及干预期的第2、4、6、8周测量各组大鼠的体质量。在治疗前后行钳夹术检测大鼠葡萄糖输注速率(GIR);治疗后通过血糖仪检测各组大鼠空腹血糖(FBG)

计算稳态模型胰岛素抵抗指数(HOMA-IR)。ELISA法检测空腹血清胰岛素(FINS)水平及肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)的含量；Western blot法检测大鼠肝脏组织TLR4/NF-κB信号通路相关因子TLR4、IκB激酶β(IKKβ)、p-IKKβ、NF-κB p65、TNF-α蛋白的表达。结果:与正常组比较，模型组各时间段体质量增加(P<0.01)

GIR水平降低(P<0.01)

HOMA-IR水平及血清FINS、TNF-α和IL-6含量升高(P<0.01)

肝脏组织中TLR4、IKKβ、p-IKKβ、NF-κB p65、TNF-α的蛋白表达增多(P<0.05)。与模型组比较，电针组从第6周开始体质量下降，治疗后GIR水平升高(P<0.01)

HOMA-IR水平及血清FINS、TNF-α和IL-6含量降低(P<0.05

P<0.01)

肝脏组织中TLR4、IKKβ、p-IKKβ、 NF-κB p65、 TNF-α的蛋白表达水平下调(P<0.05)。结论:电针可以抑制胰岛素抵抗肥胖大鼠肝脏组织中TLR4/NF-κB通路减轻炎性反应，从而提高外周胰岛素敏感性，对胰岛素抵抗肥胖有较好的调节作用。

Abstract

Objective To investigate the effect of electroacupuncture(EA) on the Toll-like receptor 4(TLR4)/nuclear factor kappa B(NF-κB) inflammatory pathway in the liver of obese rats with insulin resistance

and explore its mechanism. Methods Male Wistar rats were randomly divided into a normal group(n=15) and an experimental group(n=30). The obesity-induced insulin resistance model was induced by the high-fat diet(HFD) in rats of the experimental group for 8 weeks. Subsequently

the model rats were further divided into a model group(n=15) and an EA group(n=15). EA was applied at “Zhongwan ”(CV12)

“Guanyuan”(CV4)

“Zusanli ”(ST36) and “Fenglong ”(ST40) in the EA group for 10 min

three times a week for 8 weeks. The body weight of rats in each group was measured before intervention and at the 2

(nd)

4(nd)

(th)

6(th)

(th)

and 8(th)

and 8

(th)

weeks during the intervention. Glucose infusion rate(GIR) was measured by glucose clamp test before and after treatment. After treatment

fast blood glucose(FBG) was detected by the glucometer

and homeostasis model assessment of insulin resistance(HOMA-IR) was calculated. The contents of fasting insulin(FINS)

tumor necrosis factor-α(TNF-α)

and interleukin-6(IL-6) were determined by ELISA. The protein expressions of TLR4

IκB kinase β(IKKβ)

phosphorylated IKKβ(p-IKKβ)

NF-κB p65

and TNF-α related to the TLR4/NF-κB signaling pathway in the liver of rats were detected by Western blot. Results Compared with the normal group

the body weight

HOMA-IR levels

serum levels of FINS

TNF-α

and IL-6 were up-regulated(P

0.01)

and the GIR level was down-regulated(P

0.01)

the protein expressions of TLR4

IKKβ

p-IKKβ

NF-κB p65 and TNF-α in liver tissues were increased(P

0.05) in the model group. Compared with the model group

the EA group showed weight loss from the 6(th) weeks during the intervention. Glucose infusion rate(GIR) was measured by glucose clamp test before and after treatment. After treatment

fast blood glucose(FBG) was detected by the glucometer

and homeostasis model assessment of insulin resistance(HOMA-IR) was calculated. The contents of fasting insulin(FINS)

tumor necrosis factor-α(TNF-α)

and interleukin-6(IL-6) were determined by ELISA. The protein expressions of TLR4

IκB kinase β(IKKβ)

phosphorylated IKKβ(p-IKKβ)

NF-κB p65

and TNF-α related to the TLR4/NF-κB signaling pathway in the liver of rats were detected by Western blot. Results Compared with the normal group

the body weight

HOMA-IR levels

serum levels of FINS

TNF-α

and IL-6 were up-regulated(P

0.01)

and the GIR level was down-regulated(P

0.01)

the protein expressions of TLR4

IKKβ

p-IKKβ

NF-κB p65 and TNF-α in liver tissues were increased(P

0.05) in the model group. Compared with the model group

the EA group showed weight loss from the 6

(th)

week

and the HOMA-IR levels

serum levels of FINS

TNF-α

and IL-6 were decreased(P

0.01

0.05)

the GIR level was up-regulated(P

0.01)

the protein expressions of TLR4

IKKβ

p-IKKβ

NF-κB p65 and TNF-α in liver tissues were down-regulated(P

0.05). Conclusion EA can reduce the inflammatory response and improve peripheral insulin sensitivity by inhibiting the TLR4/NF-κB pathway in liver tissues of obese rats with insulin resistance

showing a good regulatory effect on insulin resistance induced by obesity.

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Related Institution

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Department of Rehabilitation, Wuhan Third Hospital

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