Effect of Tangnaikang on Imbalance Between NE and α<sub>1</sub>-AT in Spontaneous Type 2 Diabetic Mouse

Wen SUN; Guang-yuan XU; Dan HOU; Li-li WU

doi:10.13422/j.cnki.syfjx.20191221

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Effect of Tangnaikang on Imbalance Between NE and α₁-AT in Spontaneous Type 2 Diabetic Mouse

Pharmacology | 更新时间：2021-02-09

- Effect of Tangnaikang on Imbalance Between NE and α₁-AT in Spontaneous Type 2 Diabetic Mouse
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 22, Pages: 22-27(2019)
- 作者机构：
  
  1.北京中医药大学　中医学院，北京　 100029；
  2.首都医科大学　附属复兴医院，北京　 100038
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20191221
  CLC： R22; R242; R2-031; R285.5
- Published：20 November 2019，
  
  Published Online：04 March 2019，
  
  Received：21 January 2019，
- 稿件说明：
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Wen SUN, Guang-yuan XU, Dan HOU, et al. Effect of Tangnaikang on Imbalance Between NE and α₁-AT in Spontaneous Type 2 Diabetic Mouse. [J]. Chinese Journal of Experimental Traditional Medical Formulae 25(22):22-27(2019)
DOI：

Wen SUN, Guang-yuan XU, Dan HOU, et al. Effect of Tangnaikang on Imbalance Between NE and α₁-AT in Spontaneous Type 2 Diabetic Mouse. [J]. Chinese Journal of Experimental Traditional Medical Formulae 25(22):22-27(2019) DOI： 10.13422/j.cnki.syfjx.20191221.

摘要

目的：

观察中药糖耐康(Tangnaikang，TNK)对2型糖尿病(T2DM)的ob/ob小鼠中性粒细胞弹性蛋白酶(NE)，

-抗胰蛋白酶(

-AT)蛋白表达的调节作用。

方法：

将32只雄性SPF级ob/ob小鼠按体质量随机分为模型组(生理盐水)，TNK高剂量组(TNK溶液16.04 g·kg

－1

)，TNK中剂量组(TNK溶液8.02 g·kg

－1

)和TNK低剂量组(TNK溶液4.01 g·kg

－1

)。另取8只C57BL/6J小鼠作为正常组(生理盐水)。灌胃4周。每周记录小鼠一般状态和体质量和空腹血糖(FBG)，第25天进行口服葡萄糖耐量(OGTT)实验，第27天进行胰岛素耐量(ITT)实验，灌胃结束后，取血清检测空腹胰岛素(Fins)，NE，

-AT，取脂肪组织检测NE，

-AT，p-IRS1，葡萄糖转运蛋白4(GLUT4)蛋白表达水平。

结果：

与正常组比较，模型组ob/ob小鼠体质量显著增大，糖脂代谢指标均呈糖尿病表现，血清和脂肪组织NE显著增加(

0.01)，

-AT显著减少(

0.01)。与模型组比较，TNK高剂量组体质量，甘油三酯(TG)，总胆固醇(TC)，低密度脂蛋白(LDL)指标均显著减少(

0.01)，高密度脂蛋白(HDL)显著增加(

0.01)，FBG，Fins，胰岛素抵抗指数(HOMA-IR)，曲线下面积(AUC)

ogtt

，AUC

ITT

均显著减少(

0.01)，血清和脂肪组织NE显著减少(

0.01)，

-AT显著增加(

0.01)，脂肪组织p-IRS1和GLUT4明显增加(

0.05)。

结论：

TNK能够降低ob/ob小鼠体质量，改善糖脂代谢，升高

-AT水平，降低NE水平，调节IRS1/GLUT4信号的关键位点，可能是其改善中性粒细胞介导的脂肪组织IR的作用机制之一。

Abstract

Objective:

To observe the regulatory effect of Tangnaikang (TNK) on imbalance between neutrophil elastase (NE) and

-antitrypsin (

-AT) in ob/ob mice with type 2 diabetes mellitus (T2DM).

Method:

Thirty-two male SPF ob/ob mice were randomly divided into model group (DM

normal saline) and high-dose TNK group (TNKH

TNK solution 16.04 g·kg

-1

)

middle-dose TNK group (TNKM

TNK solution 8.02 g·kg

-1

) and low-dose TNK group (TNKL

TNK solution 4.01 g·kg

-1

). Another 8 C57BL/6J mice were included in normal group (Con

saline). The experiment lasted for four weeks. The general state

body weight (BW) and fasting blood glucose (FBG) of the mice were recorded weekly

the oral glucose tolerance (OGTT) test was performed on the 25

day

the insulin tolerance (ITT) test was performed on the 27

day

and the area under the curve (AUC) was calculated. After the end of the experiment

serum was used to detect the level of fasting insulin (Fins)

insulin resistance index (HOMA-IR)

total triglyceride (TG)

total cholesterol (TC)

high-density lipoprotein (HDL)

low-density lipoprotein (LDL)

NE and

-AT. Adipose tissue was used to detect the expressions of NE

-AT

phosphor-insulin receptor substrate 1 antibody (p-IRS1) and glucose transporter 4 (GLUT4) proteins.

Result:

Compared with the Con group

the BW of the ob/ob mice of the model group increased significantly

the glucose and lipid metabolism indexes showed diabetes

the serum and adipose tissue NE increased significantly (

0.01)

and the

-AT decreased significantly (

0.01). Compared with the DM group

the BW

and LDL indexes in the TNKH group were significantly decreased (

0.01)

the HDL was significantly increased (

0.01)

and the FBG

Fins

HOMA-IR

AUC

ogtt

and AUC

ITT

were significantly decreased (

0.01)

serum and adipose tissue NE decreased significantly (

0.01)

-AT increased significantly (

0.01)

and adipose tissue p-IRS1 and GLUT4 increased significantly (

0.05).

Conclusion:

TNK can reduce the BW of ob/ob mice

improve glycolipid metabolism

increase

-AT level

decrease NE level

and regulate IRS1-GLUT4 signaling pathway

which may be one of its mechanisms in improving IR of adipose tissue mediated by neutrophil.

关键词

2型糖尿病糖耐康ob/ob小鼠中性粒细胞弹性蛋白酶α1-抗胰蛋白酶

Keywords

type 2 diabetesTangnaikangob/ob miceneutrophil elastaseα1-antitrypsin

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Effect of Tangnaikang on Imbalance Between NE and α1-AT in Spontaneous Type 2 Diabetic Mouse

DOI：10.13422/j.cnki.syfjx.20191221

摘要

Abstract

关键词

Keywords

references

Effect of Tangnaikang on Imbalance Between NE and α₁-AT in Spontaneous Type 2 Diabetic Mouse