[1]周 宇,等.姜黄素纳米粒对高脂诱导的心肌细胞损伤的作用[J].中国药理学通报,2018,(09):1283-1288.[doi:10.3969/j.issn.1001-1978.2018.09.019]
 ZHOU Yu,LI Jing,BAO Cui-yu.Effects of curcumin nanoparticles on hyperlipid-induced cardiomyocyte injury[J].Chinese Pharmacological Bulletin,2018,(09):1283-1288.[doi:10.3969/j.issn.1001-1978.2018.09.019]
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姜黄素纳米粒对高脂诱导的心肌细胞损伤的作用()
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《中国药理学通报》[ISSN:/CN:]

卷:
期数:
2018年09期
页码:
1283-1288
栏目:
论著
出版日期:
2018-09-26

文章信息/Info

Title:
Effects of curcumin nanoparticles on hyperlipid-induced cardiomyocyte injury
文章编号:
1001-1978(2018)09-1283-06
作者:
周 宇1 2李 晶2鲍翠玉2
湖北科技学院 1.药学院、2.糖尿病心脑血管病变湖北省重点实验室,湖北 咸宁 437100
Author(s):
ZHOU Yu12 LI Jing2 BAO Cui-yu2
1.College of Pharmacy, 2.Hubei Province Key Lab on Cardiovascular, Cerebrovascular and Metabolic Disorders, Hubei University of Science and Technology, Xianning Hubei 437100, China
关键词:
姜黄素纳米粒 高脂 H9c2 心肌细胞 活性氧 凋亡
Keywords:
curcumin nanoparticles high fat H9c2 cardiomyocytes reactive oxygen apoptosis
分类号:
R282.71; R322.11; R329.24; R329.25; R587.2; R589.2; R977.6
DOI:
10.3969/j.issn.1001-1978.2018.09.019
文献标志码:
A
摘要:
目的 探讨姜黄素纳米粒(curcumin nanoparticles,Cur-NPs)对高脂诱导的心肌细胞损伤的保护作用。方法 采用棕榈酸(palmitic acid,PA)刺激H9c2心肌细胞,建立心肌细胞脂毒性损伤模型,Cur-NPs预处理,MTT法检测细胞增殖情况; 活性氧(reactive oxygen species,ROS)试剂盒检测细胞内ROS水平; TUNEL试剂盒检测细胞凋亡情况; 免疫印迹法检测细胞内质网应激和凋亡信号通路相关蛋白的表达水平。结果 高脂可引起细胞增殖率的降低,ROS水平明显升高,细胞形态出现明显的病理性损伤改变,凋亡细胞明显增多; GRP78、CHOP和caspase-3表达水平明显增加,Bax/Bcl-2的比值升高。姜黄素纳米粒可以逆转上述变化。结论 姜黄素纳米粒能够明显降低高脂诱发的心肌细胞ROS的产生,降低心肌细胞内质网应激和凋亡相关蛋白的表达,从而抑制高脂所致的H9c2心肌细胞损伤。
Abstract:
Aim To investigate the protective effect of curcumin nanoparticles(Cur-NPs)against high-fat-induced cardiomyocyte injury. Methods H9c2 cardiomyocytes were stimulated with palmitic acid(PA)to establish a rat model of lipotoxicity injury. The Cur-NPs were pretreated. MTT assay was used to detect cell proliferation. The reactive oxygen species(ROS)kit was used to detect intracellular reactive oxygen species and the cells were detected with the TUNEL kit. Apoptosis was detected by Western blot, and the expression levesl of endoplasmic reticulum stress and apoptotic signaling pathway related proteins were determined. Results High fat might cause the decrease of cell proliferation rate. The level of ROS obviously increased, and the pathological changes of cell morphology were evident. Apoptosis was obviously aggravated. The expression of GRP78, CHOP and caspase-3 apparently increased, and the Bax/Bcl-2 ratio elevated, which could all be reversed by Cur-NPs. Conclusions Cur-NPs significantly reduces the production of ROS induced by hyperlipidemia and reduces the expression of endoplasmic reticulum stress and apoptosis-related proteins in cardiomyocytes, thereby inhibiting the damage of H9c2 cardiomyocytes induced by high fat.

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备注/Memo

备注/Memo:
收稿日期:2018-04-28,修回日期:2018-05-24
基金项目:国家自然科学基金资助项目(No 51703055); 湖北省自然科学基金资助项目(No 2017CFB99,2015CFC773); 湖北省教育厅科学研究计划项目(No B201696); 湖北科技学院糖尿病专项基金(No 2016-18XZ09,14ZX-02)
作者简介:周 宇(1990-),女,硕士生,研究方向:心血管药理学,E-mail:15072191380@163.com;
鲍翠玉(1969-),女,博士,教授,研究方向:糖尿病心脑血管病变,通讯作者,E-mail:cuiyu_bao@163.com
更新日期/Last Update: 2018-08-26