Efficacy and Mechanism of Shuangyi Prescription in Improving Insulin Resistance in Type 2 Diabetes Model Rats

TIAN Chun-yu; BO Hai-mei; LIN Fei-wu; LA Xiao-jin; CAO Hui-juan; ZHU Liang; YANG Yu-yang; LI Ji-an

doi:10.13422/j.cnki.syfjx.2017220137

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Efficacy and Mechanism of Shuangyi Prescription in Improving Insulin Resistance in Type 2 Diabetes Model Rats

更新时间：2024-01-04

- Efficacy and Mechanism of Shuangyi Prescription in Improving Insulin Resistance in Type 2 Diabetes Model Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 23, Issue 22, Pages: 137-142(2017)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2017220137
  CLC： R-332;R285.5
- Published：2017
- 稿件说明：
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TIAN Chun-yu, BO Hai-mei, LIN Fei-wu, et al. Efficacy and Mechanism of Shuangyi Prescription in Improving Insulin Resistance in Type 2 Diabetes Model Rats[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(22): 137-142.
DOI：

TIAN Chun-yu, BO Hai-mei, LIN Fei-wu, et al. Efficacy and Mechanism of Shuangyi Prescription in Improving Insulin Resistance in Type 2 Diabetes Model Rats[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(22): 137-142. DOI： 10.13422/j.cnki.syfjx.2017220137.

摘要

目的：进行双益方对2型糖尿病模型大鼠的药效作用实验，分析其作用机制。方法：采用高脂饲养加25 mg · kg-1剂量链脲佐菌素腹腔注射的方法建立2型糖尿病大鼠模型，将成模动物随机分为模型组，二甲双胍组[灌胃（ig），85 mg · kg-1]，双益方高、中、低（ig，2 000，1 000，500 mg · kg-1）剂量组。进行双益方对2型糖尿病模型大鼠的体重，饮食量，饮水量，二便情况，血糖，糖耐量测定（oral glucose tolerance test，OGTT），糖化血红蛋白（hemoglobin A1c，HbA1c），糖化血清蛋白（glycosylated serum protein，GSP），胰岛素等指标的检测，蛋白免疫印迹法（Western blot）测定肝组织蛋白酪氨酸磷酸酶1B（protein tyrosine phosphatase 1B，PTP1B），蛋白激酶（Akt），磷酸化的蛋白激酶（p-Akt），糖原合成酶激酶-3β（glycogen synthase kinase-3β，GSK-3β），磷酸化的糖原合成酶激酶-3β（p-GSK-3β）的表达，Western blot测定骨骼肌组织胰岛素受体底物-1（insulin receptor substrate-1，IRS-1），磷酸化的胰岛素受体底物-1（p-IRS-1），葡萄糖转运蛋白4（glucose transporter 4，Glut4）表达的影响。结果：与模型组比较，双益方可降低2型糖尿病模型大鼠的空腹血糖（fasting blood glucose，FBG），HbAlc水平及胰岛素抵抗指数（Homa-IR），缓解2型糖尿病模型大鼠饮食量多、饮水量多、二便量大及体重减轻的状况（P<0.05，P<0.01），降低血清胰岛素、糖化血清蛋白、糖化血清蛋白及随机血糖（P<0.05，P<0.01），其中双益方高剂量组药效较好；双益方可显著升高2型糖尿病模型大鼠骨骼肌p-IRS-1，Glut4的表达（P<0.01，P<0.05）；双益方可显著升高2型糖尿病模型大鼠肝脏p-Akt的表达，显著降低PTP1B，p-GSK-3β的表达（P<0.01，P<0.05）。结论：双益方可有效调节2型糖尿病模型大鼠糖代谢紊乱，促进胰岛素分泌，改善胰岛素抵抗；调节骨骼肌PI3K/Akt，肝脏Akt/GSK-3β信号转导通路可能是该复方治疗2型糖尿病的作用机制。

Abstract

Objective: To analyze the pharmacological effect and action mechanism of Shuangyi prescription (SYP) in the treatment of type 2 diabetes rats. Method: High fat diet plus 25 mg · kg-1 streptozotocin were intraperitoneally injected to establish type 2 diabetic rats model. The model animals were randomly divided into model group

metformin group (ig

85 mg · kg-1)

SYP high dose group (ig

2 000 mg · kg-1)

SYP middle dose group (ig

1 000 mg · kg-1)

and SYP low dose group (ig

500 mg · kg-1). Body weight

food intake

water intake

urine

stool

blood glucose

oral glucose tolerance test (OGTT)

hemoglobin A1c (HbA1c)

glycosylated serum protein (GSP)

and insulin of type 2 diabetes rats were studied; Western blot was used to detect protein tyrosine phosphatase 1B (PTP1B)

Akt

p-Akt

glycogen synthase kinase-3β (GSK-3β)

p-GSK-3β expressions in liver tissues; Western blot to detect insulin receptor substrate-1 (IRS-1)

p-IRS-1

glucose transporter 4 (Glut4) expressions in skeletal muscle tissues. Result: SYP can reduce fasting blood glucose (FBG)

HbA1c level and OGTT of type 2 diabetes rats

reduce insulin resistance index. Compared with the model group

SYP can alleviate polydipsia

polyphagia

polyuria

and weight loss conditions in type 2 diabetic rats in each dose group (P<0.05

P<0.01)

SY can reduce insulin

glycated serum protein and random blood glucose (P<0.05

P<0.01)

the effect of SYP was better in the high-dose group; SYP can significantly increase p-IRS-1 and GLUT4 expressions (P<0.01

P<0.05)

reduce the expression of PTP1B (P<0.01

P<0.05) in skeletal muscles of type 2 diabetic model rats; SY can significantly increase p-Akt expression

and significantly reduce PTP1B

p-GSK-3β expressions (P<0.01

P<0.05) in liver of type 2 diabetic model rats. Conclusion: SYP can effectively regulate glycometabolic disorders in type 2 diabetes rats

improve insulin resistance. The regulation of skeletal muscle PI3K/Akt and liver Akt/GSK-3β signaling pathway may be the mechanism of SY in the treatment of type 2 diabetes.

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