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|本期目录/Table of Contents|

黄芩苷对衣霉素诱导的内质网应激性心肌细胞损伤的影响

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2014年第2期
页码:
125-128
栏目:
基础研究
出版日期:
2014-01-20

文章信息/Info

Title:
Effect of baicalin on tunicamycin-induced endoplasmic reticulum stress injury in cultured neonatal rat cardiomyocytes
作者:
杨 磊沈明志王 博郭筱王程 珂刘媛媛王晓明
(第四军医大学西京医院老年病科,陕西 西安 710032)
Author(s):
YANG Lei SHEN Ming-zhi WANG Bo GUO Xiao-wang CHENG Ke LIU Yuan-yuan WANG Xiao-ming
(Department of Geriatrics, Xijing Hospital, Fourth Military Medical University, Xi’an 710032, Shaanxi, China)
关键词:
黄芩苷衣霉素内质网应激心肌细胞大鼠
Keywords:
baicalin endoplasmic reticulum stress cardiomyocyte rats
分类号:
R-541;R284.1
DOI:
-
文献标识码:
A
摘要:
目的:观察黄芩苷(BC)对衣霉素(Tm)诱导的心肌细胞内质网应激(ERS)损伤的作用。方法: 原代新生SD大鼠心肌细胞培养,随机分为对照组、BC组、Tm组、Tm+BC组。用MTT比色法检测心肌细胞的存活率,乳酸脱氢酶(LDH)释放法检测心肌细胞损伤,原位缺口末端标记法(TUNEL)检测心肌细胞凋亡,Western blot检测CCAAT增强子结合蛋白同源蛋白(CHOP)的水平。结果: ①Tm能够损伤心肌细胞并呈现明显的时间依赖关系,各作用时间点心肌细胞的存活率差异显著(P<0.05)。Tm可显著增加ERS的CHOP表达及细胞凋亡的水平。②相对与Tm组,50 μmol/L 的BC能够显著抑制Tm对心肌细胞的损伤,使心肌细胞存活率增加(P<0.05)。同时,BC能够显著抑制Tm诱导的心肌ERS损伤,使CHOP表达及细胞凋亡的水平明显下调(P<0.05)。结论: BC可通过抑制Tm诱导的心肌ERS及心肌细胞的凋亡,达到保护受损心肌细胞的作用。
Abstract:
AIM:To investigate the effect of baicalin (BC) on endoplasmic reticulum stress (ERS) tunicamycin-induced cardiomyocyte injury. METHODS: Tunicamycin (Tm) was used to establish the model of endoplasmic reticulum stress in cultured neonatal rat cardiomyocytes, which were divided into four groups: control group, BC group, Tm group and BC+Tm group. MTT assay was used to detect cell viability, LDH release and TUNEL assay were applied to determine cell damage, and Western blot was used to detect protein expressions of C/EBP-homologous protein (CHOP). RESULTS: Tm damaged the myocardial cell in a time-dependent manner, which showed significant differences from those in the normal group at all timepoints (P<0.05). Tm significantly increased the CHOP expression of ERS and apoptosis level. Presence of BC (50 μmol/L) markedly improved cell viability against Tm-induced myocardial cell injury when compared with Tm group (P<0.05). BC significantly lowered the expression of CHOP and apoptosis, which inhibited ERS Tm-induced injury in cultured neonatal rat cardiomyocytes (P<0.05). CONCLUSION: Baicalin protects cardiomyocytes against Tm-induced injury through attenuation of ERS.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期:2013-11-16.
基金项目:国家自然科学基金项目资助(81070127);军队保健专项科研课题项目资助(13BJZ34);陕西省社会发展项目资助(2012K19-05-02)
通讯作者:王晓明,主任医师,主要从事心血管疾病基础与临床研究Email:xmwang@fmmu.edu.cn
作者简介:杨磊,住院医师,硕士Email: yanglei_fmmu_2011@163.com
更新日期/Last Update: 2014-01-16