Anti-hyperlipidemia Effect of Shuanghuang Tiaozhi Prescription by Regulating CHO and TG Metabolism

XUAN Ying-mei; ZHANG Guang-ping; MA Li-na; SU Ping; HOU Hong-ping; YANG Yi-fei; YE Zu-guang

doi:10.13422/j.cnki.syfjx.2017100079

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Anti-hyperlipidemia Effect of Shuanghuang Tiaozhi Prescription by Regulating CHO and TG Metabolism

更新时间：2024-01-04

- Anti-hyperlipidemia Effect of Shuanghuang Tiaozhi Prescription by Regulating CHO and TG Metabolism
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 23, Issue 10, Pages: 79-84(2017)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2017100079
  CLC： R285.5
- Published：2017
- 稿件说明：
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XUAN Ying-mei, ZHANG Guang-ping, MA Li-na, et al. Anti-hyperlipidemia Effect of Shuanghuang Tiaozhi Prescription by Regulating CHO and TG Metabolism[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(10): 79-84.
DOI：

XUAN Ying-mei, ZHANG Guang-ping, MA Li-na, et al. Anti-hyperlipidemia Effect of Shuanghuang Tiaozhi Prescription by Regulating CHO and TG Metabolism[J]. Chinese journal of experimental traditional medical formulae, 2017, 23(10): 79-84. DOI： 10.13422/j.cnki.syfjx.2017100079.

摘要

目的：通过体内外实验研究双黄调脂方的降脂作用，探讨其降脂机制。方法：昆明种小鼠随机分为正常组、模型组、阳性药组（血脂康，0.6 g·kg-1）和双黄调脂高、低剂量组（22.5，7.5 g·kg-1），观察双黄调脂方对Trtion-WR1339诱导的高血脂模型的影响。基于整体实验，体外实验观察了双黄调脂主要有效成分姜黄素、黄连素、葛根素对油酸（oleic acid，OA）诱导的HepG2细胞模型胆固醇（CHO），甘油三酯（TG），3-羟基-3-甲基戊二酰CoA（HMG-CoA）还原酶，高密度脂蛋白胆固醇（HDL-C），低密度脂蛋白受体（LDL-R），胆固醇7α-羟化酶（CYP7A1）和脂蛋白脂酶（LPL）含量的影响，探讨其可能降脂途径。结果：与正常组比较，模型组小鼠血清CHO和TG含量显著升高（P<0.01）；与模型组比较，双黄调脂方高剂量组能显著降低模型小鼠血清的CHO，TG水平（P<0.05，P<0.01）。体外实验中，与空白组比较，模型组细胞CHO，TG和HMG-CoA还原酶含量显著升高（P<0.05，P<0.01），HDL-C，LDL-R，CYP7A1和LPL含量显著降低（P<0.05）；与模型组比较，姜黄素高剂量组（10 mg·L-1）能显著升高模型细胞HDL-C，LDL-R和LPL含量（P<0.05，P<0.01），降低TG和HMG-CoA含量（P<0.05，P<0.01）；黄连素高剂量组（40 mg·L-1）能显著升高模型细胞CHO，HDL-C，LDL-R和CYP7A1含量（P<0.05，P<0.01）；葛根素高剂量组（300 mg·L-1）能显著升高模型细胞HDL-C，LDL-R，CYP7A1和LPL含量（P<0.05，P<0.01），降低CHO，TG和HMG-CoA含量（P<0.05，P<0.01）。结论：双黄调脂方可通过抑制内源性胆固醇合成、促进胆固醇逆转运（RCT）途径和低密度脂蛋白（LDL）受体途径、促进胆固醇转化以及促进甘油三酯降解等多个途径来发挥降脂作用。

Abstract

Objective: To study the effect of Shuanghuang Tiaozhi prescription in vivo and in vitro

in order to explore its lipid-lowering mechanism. Method: KM mice were randomly divided into normal control group

model group

positive drug group (Xuezhikang

0.6 g·kg-1)

high and low-dose Shuanghuang Tiaozhi prescription groups (22.5

7.5 g·kg-1). The effects of Shuanghuang Tiaozhi prescription on hyperlipidemic rat models induced by Triton-WR 1339 were studied. Based on the experiment in vivo

the effects of curcumin

berberine and puerarincan on the contents of cholesterol (CHO)

triglyceride (TG)

3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase

high density lipoprotein cholesterol (HDL-C)

low-density lipoprotein receptor (LDL-R)

cholesterol 7a-hydroxylase (CYP7A1) and lipoprotein lipase (LPL) in HepG2 cells induced by oleic acid (OA) were studied to explore the ways of reducing blood lipid. Result: Compared with normal control group

serum CHO and TG content of model mice were significantly increased (P<0.01). Compared with model group

high-dose Shuanghuang Tiaozhi prescription (22.5 g·kg-1) can significantly decrease serum CHO and TG content of model mice (P<0.05

P<0.01). In vitro

compared with normal control group

CHO

TG and HMG-CoA reductase content of model cells significantly increased (P<0.05

P<0.01)

HDL-C

LDL-R

CYP7A and LPL content of model cells were significantly decreased (P<0.05). Compared with model group

high-dose curcumin (10 mg·L-1) can significantly increase HDL-C

LDL-R

LPL content and decrease TG

HMG-CoA content in model cells (P<0.05

P<0.01); high-dose berberine (40 g·L-1) can significantly increase CHO

HDL-C

LDL-R

CYP7A1 content in model cells (P<0.05

P<0.01); high-dose puerarincan (300 mg·L-1) can significantly increase HDL-C

LDL-R

CYP7A1

LPL content and decrease CHO

HMG-CoA content in model cells (P<0.05

P<0.01). Conclusion: Shuanghuang Tiaozhi prescription can reduce blood lipid by inhibiting endogenous cholesterol synthesis

promoting RCT and LDL receptor pathway

cholesterol transformation and degradation of triglyceride.

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