HMGB1在脓毒症心肌损害小鼠中的表达及炎症促进作用研究

冯宣云; 艾山木; 刘琼

doi:10.13406/j.cnki.cyxb.001294

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HMGB1在脓毒症心肌损害小鼠中的表达及炎症促进作用研究

基础研究 | 更新时间：2024-01-17

- HMGB1在脓毒症心肌损害小鼠中的表达及炎症促进作用研究
- Expression of HMGB1 in sepsis myocardial injury and its role in promoting inflammation
- 重庆医科大学学报 2017年42卷第5期页码：509-514
- 作者机构：
  
  重庆医科大学附属第一医院急诊医学科&重症医学科
- 作者简介：
- 基金信息：
- DOI：10.13406/j.cnki.cyxb.001294
  中图分类号： R459.7
- 纸质出版日期：2017，
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冯宣云, 艾山木, 刘琼. HMGB1在脓毒症心肌损害小鼠中的表达及炎症促进作用研究[J]. 重庆医科大学学报, 2017,42(5):509-514.

Feng Xuanyun, Ai Shanmu, Liu Qiong. Expression of HMGB1 in sepsis myocardial injury and its role in promoting inflammation[J]. Journal of Chongqing Medical University, 2017,42(5):509-514.
冯宣云, 艾山木, 刘琼. HMGB1在脓毒症心肌损害小鼠中的表达及炎症促进作用研究[J]. 重庆医科大学学报, 2017,42(5):509-514. DOI： 10.13406/j.cnki.cyxb.001294.

Feng Xuanyun, Ai Shanmu, Liu Qiong. Expression of HMGB1 in sepsis myocardial injury and its role in promoting inflammation[J]. Journal of Chongqing Medical University, 2017,42(5):509-514. DOI： 10.13406/j.cnki.cyxb.001294.

摘要

目的:探究高迁移率族蛋白B1(high mobility group box-1 protein

HMGB1)在脓毒症心肌损害(sepsis induced myocardial depression

SIMD)中的表达以及通过HMGB1抑制剂甘草酸(glycyrrhizin

GL)在SIMD中的作用。方法:将小鼠分为正常组、盲肠结扎穿孔(cecal ligation and puncture

CLP)模型组、CLP+PBS对照组和CLP+GL干预组

每组随机分配5只C57BL/6雄性小鼠

通过ELISA检测小鼠血清、心脏匀浆液中高迁移率族蛋白B1(high mobility group box-1 protein

HMGB1)的表达

RT-PCR对小鼠心肌组织中HMGB1进行定量分析

使用GL干预CLP小鼠模型后检测外周血中肿瘤坏死因子-α(tumor necrosis factor-α

TNF-α)、白介素-1β(interleukin-1β

IL-1β)、IL-6、IL-10、IL-33等细胞因子水平变化。结果:(1)CLP诱导SIMD小鼠模型中

HMGB1以及心肌损害标志物c TnⅠ的表达较正常对照组明显升高(P<0.05);(2)GL处理SIMD小鼠模型后

TNF-α、IL-1β、IL-6、IL-10、IL-33等细胞因子以及心肌损害标志物c TnⅠ表达较对照组和模型组明显降低(P<0.01)。结论:抑制HMGB1可降低机体各种炎症因子水平

调控脓毒症的失控性炎症效应

减轻脓毒症心肌损害。

Abstract

Objective:To explore expression of high mobility group box-1 protein（HMGB1）in sepsis induced myocardial depression（SIMD）and the role of inhibiting glycyrrhizic（GL）in SIMD. Methods:Mice were divided into normal group

cecal ligation and perforation（cecal ligation and puncture

CLP）model group

CLP+PBS control group and CLP+GL group

each group were randomly assigned to 5 male C57BL/6 mice. Expressions of HMGB1 ELISA in serum

heart homogenate

RT-PCR of HMGB1 in myocardial tissue of mice were detected by quantitative analysis of changes the factor level in peripheral blood of tumor necrosis factor-α（TNF-α）

interleukin-1β（IL-1β）

IL-6

IL-10 and IL-33 cells were detected by GL CLP mice after intervention. Results:CLP induced mouse model of SIMD. HMGB1 and myocardial damage marker expression in c TnⅠ was obviously higher than that of normal control group（P<0.05）. SIMD mice model of GL after treatment

TNF-α

IL-1β

IL-6

IL-10

IL-33 cytokines

myocardial damage marker c Tn I expression was significantly lower than that of control group and the model group（P<0.01）. Conclusion:Inhibiting HMGB1 can reduce the level of inflammatory factors in the body

control the uncontrolled inflammatory effect of sepsis

and reduce the myocardial damage in sepsis.

关键词

高迁移率族蛋白B1脓毒症心肌损害炎症因子

Keywords

high mobility group box protein B1sepsis myocardial damageinflammatory cytokines

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