首页
期刊简介
编 委 会
期刊订阅
百年学会 医星璀璨
名院风范
学科风华
菁英风采
投稿须知
过刊浏览
联系我们
篇名
关键词
作者
作者单位
摘要
关键词
注册本刊作者
作者投稿查稿
专家远程审稿
编辑在线审稿
编务办公专区
主编办公专区
下载文档
《上海医学》审稿费代缴委托书
《上海医学》杂志2024年征订启事回执
《上海医学》期刊编审系统审稿专家使用手册
工作动态
03-05
《上海医学》杂志2024年度“春蕾杯”论文评比征文通知
06-14
创新驱动,培育人才—《上海医学》2021年度春蕾计划评审结果揭晓
01-21
《上海医学》期刊影响力指标和学科排名取得显著提升
01-20
《上海医学》恭祝大家新年快乐!
08-18
作废声明
联系方式
发行周期:
月刊
主管单位:
上海市卫生健康委员会
主办单位:
上海市医学会
编辑出版:
《上海医学》编辑部
联系地址:
上海市北京西路1623号
邮编:
200040
电话:
021-62178606
传真:
021-62178606
邮箱:
smasmj@shsma.org.cn
ISSN:
ISSN0253-9934
CN:
CN31-1366/R
收款账号:
1001255309008900719
账户名:
上海市医学会
开户行:
工商银行上海市静安寺支行
友情链接
上海市医学会
当前位置:首页 >
芪苈强心对心肌梗死后心力衰竭大鼠mRNA表达谱的调控作用
Impact of Qiliqiangxin on gene expression profiling in rats with post-infarction heart failure
浏览(1146) 下载(2)
DOI:
作者:
张敬敬
Zhang Jingjing
作者单位:
山东大学
Shandong University Jinan 250013, China
关键词:
芪苈强心;心肌梗死后心力衰竭;mRNA芯片
Qiliqiangxin; Post-infarction heart failure; Microarray
摘要:
【摘要】目的:通过基因芯片技术研究芪苈强心对心肌梗死后心力衰竭大鼠心肌组织基因表达谱的影响,并进行生物信息学分析,从而揭示芪苈强心的作用靶点和相关通路。方法:通过结扎SD大鼠冠状动脉左前降支建立心肌梗死后心力衰竭模型。将实验动物随机分为假手术组(Sham)、心梗后心衰模型组(Control)和芪苈强心组(QL),干预6周后行超声心动图检测及组织病理学分析。取梗死边缘区心肌组织进行基因芯片杂交,筛选差异表达mRNA,进行生物信息学分析(包括GO功能富集分析和KEGG通路富集分析),并对参与重要信号通路的差异表达基因进行RT-PCR验证。结果:Control组较Sham组左心室收缩功能显著降低,HE染色示炎症细胞浸润显著增加(p<0.01)。给予芪苈强心干预后,心衰大鼠心功能显著改善,炎症细胞浸润显著减少(p<0.01)。基因芯片结果显示,与Sham组相比,Control组上调的基因有619个,下调的基因有308个;与Control组相比,QL组上调的基因有124个,下调的基因有436个。3组共同差异表达的基因有385个。GO分析显示差异表达基因富集于生物学过程(共758个条目)、细胞组分(共54个条目)和分子功能(共78个条目)3个分类,涉及的细胞生物学行为主要集中在趋化因子活性、炎症应激反应,细胞增殖调节、外泌体功能等方面;KEGG分析结果显示,差异表达基因在31个分子通路中得到富集,包括趋化因子信号转导通路、补体途径、AGE-RAGE信号通路、HIF-1信号通路、糖酵解通路等相关通路。对趋化因子信号通路的9个差异表达基因进行mRNA水平验证,RT-PCR结果与基因芯片结果具有较好的一致性。结论:芪苈强心通过调节一系列的基因和通路来保护心肌梗死后心力衰竭大鼠的心脏功能。
[Abstract] Objective: The present study aims to investigate the impact of Qiliqaingxin(QL) on gene expression profiling in rat model of post-infarction heart failure by microarray technology and bioinformatic analysis, so as to explore possible targets and pathways of QL treatment.Methods: Post-infarction heart failure model was established by ligation of left anterior descending coronary artery in SD rats. Animals were then randomly divided into Sham group, Control group and QL-treated group. Echocardiography and histological study were performed after 6 weeks of intervention. Peri-infarct myocardial tissues were subjected to microarray hybridization for screening of differentially expressed genes, followed by bioinformatic analysis including Gene Ontology ( GO) and Kyoto Encyclopedia of Genes and Genomes ( KEGG) enrichment analysis. Genes that participated in critical signaling pathways were validated by real-time quantitative polymerase chain reaction (RT-PCR). Results: Compared with sham group, significantly reduced left ventricular systolic function and increased inflammatory cell infiltrates exhibited by HE staining could be observed in control group (p<0.01). While QL improved the cardiac function and inhibited the inflammatory cell infiltration significantly(p<0.01). Compared with Sham group, there were 621 genes significantly up-regulated and 308 down-regulated in Control group; while in comparison with Control group, 124 genes were up-regulated and 436 down-regulated in QL group. A total of 385 genes were commonly differentially expressed in all three groups. GO enrichment analysis demonstrated that these commonly differentially expressed genes were enriched in the three aspects of biological process (758 categories), cellular component (54 categories) and molecular function (78 categories), mostly focused on chemokine activity, inflammatory and stress response, regulation of cell proliferation, extracellular exosome, etc. KEGG pathway enrichment analysis indicated that differentially expressed genes were significantly enriched in 31 signaling pathways, including chemokine signaling pathway, complement and coagulation cascades, AGE-RAGE signaling pathway, HIF-1 signaling pathway, and glycolysis, etc. 9 differentially expressed genes in chemokine signaling pathway were validated by RT-PCR and consistent with gene microarray results. Conclusion: QL protected cardiac function against post-infarction heart failure via multiple genes and signaling pathways.
点击下载DOC全文