红景天苷改善糖尿病大鼠肝脏糖脂水平的作用机制

候丹; 许光远; 张茁; 刘铜华

doi:10.13422/j.cnki.syfjx.20182124

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红景天苷改善糖尿病大鼠肝脏糖脂水平的作用机制

药理 | 更新时间：2021-02-09

- 红景天苷改善糖尿病大鼠肝脏糖脂水平的作用机制
- Mechanism of Salidroside in Improving Glucose and Lipid Metabolism in Liver of Diabetic Rats
- 中国实验方剂学杂志 2019年25卷第1期页码：130-134
- 作者机构：
  
  1.北京中医药大学　中医养生学北京市重点实验室，北京　 100029
  2.首都医科大学　附属复兴医院，北京　 100045
- 作者简介：
  
  候丹，硕士，从事中医药防治糖尿病及其并发症的临床和基础研究，Tel：010-64286950，E-mail：859669724@qq.com
  刘铜华，教授，博士生导师，从事中医药防治糖尿病及其并发症的临床和基础研究，Tel：010-64286950，E-mail: thliu@vip.163.com
- 基金信息：
  
  国家“十二五”科技支撑计划项目(2014BAI10B04)
- DOI：10.13422/j.cnki.syfjx.20182124
  中图分类号： R22;R242;R2-031;R285.5
- 收稿日期：2018-05-09，
  
  网络出版日期：2018-08-24，
  
  纸质出版日期：2019-01-05
- 稿件说明：
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候丹, 许光远, 张茁, 等. 红景天苷改善糖尿病大鼠肝脏糖脂水平的作用机制[J]. 中国实验方剂学杂志, 2019,25(1):130-134.

Dan HOU, Guang-yuan XU, Zhuo ZHANG, et al. Mechanism of Salidroside in Improving Glucose and Lipid Metabolism in Liver of Diabetic Rats[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(1): 130-134.
候丹, 许光远, 张茁, 等. 红景天苷改善糖尿病大鼠肝脏糖脂水平的作用机制[J]. 中国实验方剂学杂志, 2019,25(1):130-134. DOI： 10.13422/j.cnki.syfjx.20182124.

Dan HOU, Guang-yuan XU, Zhuo ZHANG, et al. Mechanism of Salidroside in Improving Glucose and Lipid Metabolism in Liver of Diabetic Rats[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(1): 130-134. DOI： 10.13422/j.cnki.syfjx.20182124.

摘要

目的：

探讨红景天苷对糖尿病大鼠肝脏糖脂代谢作用机制。

方法：

6～7周龄雄性Zucker糖尿病（ZDF）（fa/fa）大鼠24只，按照血糖随机分为模型组，红景天苷低剂量组（0.05 g·kg

－1

），红景天苷高剂量组（0.1 g·kg

－1

），8只/组，另选同周龄ZDF （fa/+）大鼠8只为正常组，连续给药干预6周。实验结束后，检测大鼠空腹血糖（fasting blood glucose

FBG），甘油三酯（triglyceride

TG），总胆固醇（total cholesterol

TC），游离脂肪酸（free fatty acids

FFA），超氧化物酶歧化酶（superoxide dismutase

SOD），丙二醛（malondialdehyde

MDA），过氧化氢酶（catalase

CAT），血清胰岛素水平（fasting insulin

Fins），胰岛素抵抗指数（homeostasis model assessment insulin resistance

HOMA-IR）；蛋白免疫印迹法（Western blot）检测肝脏蛋白激酶样内质网激酶（PKR-like ER kinase

PERK），核转录因子2相关因子2（NF-E2-relatedfactor2，Nrf2），血红素氧化酶-1（heme oxidase-1，HO-1）蛋白表达。

结果：

与正常组比较，模型组大鼠FBG

Fins

HOMA-IR

FFA

MDA明显升高（

0.05，

0.01）；SOD

CAT明显降低（

0.05，

0.01）；肝脏p-PERK

Nrf2，HO-1蛋白表达明显降低（

0.05，

0.01）。与模型组比较，红景天苷高、低剂量组大鼠FBG

Fins

HOMA-IR

FFA

MDA明显降低（

0.05，

0.01）；SOD

CAT明显升高（

0.05，

0.01）；肝脏p-PERK

Nrf2，HO-1蛋白表达明显升高（

0.05，

0.01）。

结论：

红景天苷能够改善糖尿病大鼠糖脂水平、胰岛素抵抗，可能是通过上调p-PERK

Nrf2，HO-1蛋白表达，抑制氧化应激实现的。

Abstract

Objective:

To explore the mechanism of salidroside(SAL) in improving glucose and lipid metabolism in liver of diabetic rats.

Method:

According to blood glucose

24 male ZDF(fa/fa) rats of 6-7 week old were randomly divided into model group

SAL-low group (0.05 g·kg

-1

)

SAL-high group (0.1 g·kg

-1

)

8 rats in each group. Another 8 ZDF (fa/+ ) rats were selected as normal group. All the rats were administered continuously for 6 weeks. After experiment

fasting blood glucose(FBG)

triglyceride(TG)

total cholesterol(TC)

free fatty acids(FFA)

superoxide dismutase (SOD)

malondialdehyde (MDA)

catalase (CAT)

fasting insulin(Fins)

and homeostasis model assessment insulin resistance(HOMA-IR) were measured. Western blot was used to detect phosphorylated PKR-like ER kinase(p-PERK)

NF-E2-relatedfactor2(Nrf2)

heme oxidase-1(HO-1) protein expression levels in liver.

Result:

As compared with normal group

FBG

Fins

HOMA-IR

FFA

and MDA were increased significantly in model group (

0.05

0.01)

while SOD

CAT levels were significantly decreased (

0.05

0.01); the protein expression levels of p-PERK

Nrf2

and HO-1 in control group were significantly decreased in model group(

0.05

0.01). As compared with model group

FBG

Fins

HOMA-IR

FFA

and MDA levels were decreased significantly (

0.05

0.01)

while SOD and CAT levels were significantly increased in SAL low and high groups (

0.05

0.01); and the protein expression levels of p-PERK

Nrf2

and HO-1 in SAL group were significantly increased(

0.05

0.01).

Conclusion:

The Salidroside can improve metabolism of glucose and lipid

IR in diabetic rats

and the mechanism may be associated with inhabiting oxidative stress through the up-regulation of p-PERK

Nrf2

and HO-1 protein expression.

关键词

Keywords

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