EGCG抗糖尿病心肌病小鼠心肌组织中氧化应激损伤作用机制的探讨

任仲坤; 张志毕; 刘艳红; 张荣平; 杨晖

doi:10.13422/j.cnki.syfjx.2018030148

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EGCG抗糖尿病心肌病小鼠心肌组织中氧化应激损伤作用机制的探讨

药理 | 更新时间：2024-01-04

- EGCG抗糖尿病心肌病小鼠心肌组织中氧化应激损伤作用机制的探讨
- Anti-inflammatory and Anti-oxidative Stress Damage of Catechin Gallate on Diabetic Myocardial in C57 Mice
- 中国实验方剂学杂志 2018年24卷第3期页码：148-153
- 作者机构：
- 作者简介：
- 基金信息：
  
  云南省教育厅指导性项目（2017ZDX157）;云南省科技厅-昆明医科大学联合专项（2015FB010）;南药协同创新项目（2011）;昆明医科大学本科生创新项目
- DOI：10.13422/j.cnki.syfjx.2018030148
  中图分类号： R285.5
- 纸质出版日期：2018
- 稿件说明：
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任仲坤, 张志毕, 刘艳红, 等. EGCG抗糖尿病心肌病小鼠心肌组织中氧化应激损伤作用机制的探讨[J]. 中国实验方剂学杂志, 2018,24(3):148-153.

REN Zhong-kun, ZHANG Zhi-bi, LIU Yan-hong, et al. Anti-inflammatory and Anti-oxidative Stress Damage of Catechin Gallate on Diabetic Myocardial in C57 Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(3): 148-153.
任仲坤, 张志毕, 刘艳红, 等. EGCG抗糖尿病心肌病小鼠心肌组织中氧化应激损伤作用机制的探讨[J]. 中国实验方剂学杂志, 2018,24(3):148-153. DOI： 10.13422/j.cnki.syfjx.2018030148.

REN Zhong-kun, ZHANG Zhi-bi, LIU Yan-hong, et al. Anti-inflammatory and Anti-oxidative Stress Damage of Catechin Gallate on Diabetic Myocardial in C57 Mice[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(3): 148-153. DOI： 10.13422/j.cnki.syfjx.2018030148.

摘要

目的：探讨儿茶素没食子酸酯（EGCG）对糖尿病小鼠高糖诱导的心肌组织氧化应激损伤的影响。方法：采用雄性C57小鼠给予高糖高脂饮食6周后，按70 mg·kg-1的标准腹腔注射链脲佐菌素（STZ），连续5 d。空腹血糖（FBG）>16.7 mmol·L-1视为造模成功。后随机分为空白组，模型组，EGCG低、中、高剂量组（50，100，200 mg·kg-1），N-乙酰半胱氨酸（NAC，100 mg·kg-1）组，腹腔注射，隔天1次，连续4周。分别测定小鼠体重、心脏质量、心脏质量指数、血糖值；镜下观察心肌细胞及组织病理变化；酶联免疫吸附法（ELISA）检测心肌组织活性氧（ROS），超氧化物歧化酶（SOD），丙二醛（MDA）及炎性因子白细胞介素（IL）-1β，IL-6，肿瘤坏死因子（TNF）-α的含量；蛋白免疫印迹法（Western blot）测定心肌组织中NF-E2相关因子2（Nrf2）介导的抗氧化通路中血红素氧合酶-1（HO-1）和醌氧化还原酶1（NQO1）的表达。结果：与模型组相比，EGCG （100 mg·kg-1）组能一定程度降低血清中的FBG水平（P<0.05）；抑制心肌细胞肥大及心肌组织纤维化程度，增强SOD活性，降低MDA，ROS含量（P<0.05）；降低组织中炎性因子IL-1β，IL-6，TNF-α的含量（P<0.05）；激活心肌细胞核内Nrf2介导的抗氧化通路，作用优于强抗氧化剂NAC。结论：EGCG对高糖诱导的心肌细胞损伤具有保护作用，其机制可能与EGCG的抗氧化应激、抗炎作用有关。

Abstract

Objective:To explore the protective effect of catechin gallate (EGCG) on diabetic myocardial injury in C57 mice. Method:The diabetic cardiomyopathy injury model in C57 mice was induced by injected with streptozocin (STZ

70 mg·kg-1) and provided with high-diet food. The DCM mice were randomly divided into 6 groups

namely blank group

model group

EGCG group (50

100

200 mg·kg-1)

and N-acetyl-L-cysteine(NAC) group (100 mg·kg-1). Each group was put to death on the 14th day after intraperitoneal injection. The level of fasting blood-glucose (FBG) was detected by kit; reactive oxygen (ROS)

malondialdehyde (MDA)

superoxide dismutase (SOD)

interniukin (IL)-1β

IL-6 and tumor necrosis factor (TNF)-α were measured by enzyme linked immunosorbent assay (ELISA) kit. Myocardial pathological changes of cardiomyopathy injury were observed under microscope; Nrf2 and HO-1

NQO1 protein kinases were detected by Western blot. Result:Compared with the model group

EGCG (100 mg·kg-1) can decrease the level of FBG in DCM C57 mice and inhibit the activities of IL-1β

IL-6

MDA

ROS in cardiac muscle tissues (P<0.05); increase the activity of SOD in cardiac muscle tissues (P<0.05); increase the expression of protein kinase of Nrf2

HO-1

NQO1 in cardiac muscle tissues (P<0.05). Moreover

EGCG (100 mg·kg-1) can restrain the cardiomyocyte hypertrophy and interstitial fibrosis apparently in cardiac muscular tissues. The findings showed that EGCG was better than NAC. Conclusion:EGCG has a protective effect on diabetic cardiomyopathy in C57 mice. The mechanism may be correlated with its anti-inflammatory and anti-oxidative stress damage action.

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