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中国临床药理学与治疗学 ›› 2010, Vol. 15 ›› Issue (3): 287-291.

• 专论 • 上一篇    下一篇

大黄素对心肌梗死后小鼠心肌组织TNF-α、IL-10 基因表达和NF-κB活性的影响

吴艳霞1, 付雷2, 黄浩2   

  1. 1武汉第一医院老年病科;2武汉第一医院中心实验室, 武汉430022, 湖北
  • 收稿日期:2010-02-05 修回日期:2010-02-05 发布日期:2020-10-14
  • 通讯作者: 黄浩, 男, 博士, 副主任医师, 主要从事中药在抗炎及感染性疾病方面的机制研究。E-mail:whhuanghao10 @yahoo.com.cn
  • 作者简介:吴艳霞, 女, 博士, 副主任医师, 主要从事老年病方面的研究。Tel:13871557955 E-mail:spring-w@126.com
  • 基金资助:
    武汉科技晨光计划(20055003059-39)

Effect of emodin on TNF-αand IL-10 gene expressions and the NF-κBactivityin the myocardial tissue after myocardial infarction in mice

WU Yan-xia1, HUANG Hao2, FU Lei2   

  1. 1Department of Senile Disease, Wuhan First Hospital;2Center of Experimental Medicine, Wuhan First Hospital, Wuhan 430022, Hubei, China
  • Received:2010-02-05 Revised:2010-02-05 Published:2020-10-14

摘要: 目的: 研究大黄素对小鼠缺血后心肌局部细胞因子TNF-α和IL-10 表达及NF-κB 活性的影响。方法: 持续性结扎小鼠冠状动脉左前降支造成心肌缺血损伤模型, 用大黄素进行干预。实时定量PCR 检测干预后心肌组织的TNF-α和IL-10 的mRNA, ELISA 法检测TNF-α和IL-10蛋白水平, EMSA 测定NF-κB 的活性。结果: 经大黄素干预后, 心肌组织TNF-α的表达明显减少(P<0.01), IL-10 的表达增加(P<0.01), I L-10/TNF-α的比值显著性升高, NF-κB 的活性明显减弱(P<0.01)。结论: 大黄素显著抑制干预后心肌组织促炎性细胞因子的表达, 抑制NF-κB 的活性。

关键词: 大黄素, 核因子-κB, 心肌缺血

Abstract: AIM: To study the effect of emodin on TNF-and I L-10 g ene ex pressions and the NF-B activity in the myocardial tissue after myocardial infarction in mice. METHODS: The my ocardiali schemia damage model was caused by sustained left anterior descending coro nary artery ligation in mice and em odin was used to intervene with. The mRNA and protein expression levels of TNF-αand IL-10 in my ocardial tissue af teremodin intervention were detected by fluore scence quanti tative RT-PCR and ELISA.The activity of NF-κB in myocardial tissue was detected by elect rophoretic mo bility shift assay. RESULTS: After intervent ion by emodin, the expression of TNF-αwas signif icant ly reduced and the expression of IL-10 and ratios of IL-10/TNF-αwe resig nificantly increased in the my ocardial tissue of my ocardial infarction damage model. CONCLUSION: Emodinsig nificantly inhibits the expression of pro-inflammatory cytokines and the activity of NF-κB in myocardial tissue.

Key words: Emodin, NF-κB, My ocardial ischemia

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