中国组织工程研究 ›› 2012, Vol. 16 ›› Issue (28): 5149-5153.doi: 10.3969/j.issn.2095-4344.2012.28.005

• 血管组织构建 vascular tissue construction • 上一篇    下一篇

二氮嗪预处理缺氧复氧大鼠心肌微血管内皮细胞PI3K、Akt、FKN mRNA的表达

张永华,陈秋萍,曹 苏,沈施仁   

  1. 南通大学附属医院麻醉科,江苏省南通市 226001
  • 收稿日期:2011-12-08 修回日期:2011-12-31 出版日期:2012-07-08 发布日期:2012-07-08
  • 通讯作者: 曹苏,主任医师,南通大学附属医院麻醉科,江苏省南通市 226001 mzkcs@sina.com
  • 作者简介:张永华★,男,1978年生,江苏省通州市人,汉族,2007年徐州医学院毕业,硕士,主治医师,主要从事重要脏器功能保护的研究。 g6115206@163.com

Effects of diazoxide pretreatment on the mRNA expression of PI3K, Akt, and FKN in rat myocardium microvascular endothelial cells exposed to hypoxia-reoxygenation

Zhang Yong-hua, Chen Qiu-ping, Cao Su, Shen Shi-ren   

  1. Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China
  • Received:2011-12-08 Revised:2011-12-31 Online:2012-07-08 Published:2012-07-08
  • Contact: Cao Su, Chief physician, Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China 226001.mzkcs@sina.com
  • About author:Zhang Yong-hua★, Master, Attending physician, Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong 226001, Jiangsu Province, China g6115206@163.com

摘要:

背景:在缺氧复氧早期,促使心肌微血管内皮细胞增殖的措施,涉及一系列相关基因的改变和受多种基因调控。
目的:观察二氮嗪预处理对缺氧复氧大鼠心肌微血管内皮细胞增殖和PI3K、Akt和FKN mRNA表达的影响。
方法:培养SD大鼠心肌微血管内皮细胞,按照不同的干预方式将细胞随机均分为正常对照组、缺氧/复氧组、二氮嗪组、二氮嗪+阻断剂组。观察凋亡细胞形态、活力及PI3K、Akt和FKN mRNA转录水平。
结果与结论:与正常对照组比较,缺氧/复氧组细胞增殖率显著降低、Akt和FKN显著升高(P < 0.01)。与缺氧/复氧组比较,二氮嗪组细胞增殖率显著升高(P < 0.05);PI3K和Akt 显著升高、FKN显著降低(P < 0.01)。二氮嗪+阻断剂组取消了二氮嗪的作用,与缺氧/复氧组比较差异无显著性意义。说明二氮嗪预处理通过促使细胞增殖,上调PI3K、Akt mRNA表达、下调FKN mRNA表达而实现对缺氧复氧心肌微血管内皮细胞损伤的保护。

关键词: 二氮嗪, 心肌微血管内皮细胞, PI3K, Akt, FKN, 缺氧复氧

Abstract:

BACKGROUND: In the early stage of hypoxia-reoxygenation, the measures of promoting proliferation myocardium microvascular endothelial cells (MMECs) involve a series of related genetic changes, which are regulated by multiple genes.
OBJECTIVE: To investigate the effects of diazoxide pretreatment on the mRNA expression of PI3K, Akt and FKN as well as proliferation of rat MMECs exposed to hypoxia-reoxygenation.
METHODS: The SD rat MMECs were randomly divided into normal control group, hypoxia-reoxygenation group, diazoxide pretreatment group and diazoxide pretreatment+5-hydroxydecanoate group. Cell vitality, morphology, apoptotic rate and mRNA expression of PI3K, Akt and FKN were detected.
RESULTS AND CONCLUSION: Compared with the normal control group, the cell proliferation rate was significantly decreased and the mRNA expression of FKN and Akt was up-regulated in the hypoxia-reoxygenation group (P < 0.01). Compared with the hypoxia-reoxygenation group, the cell proliferation rate was significantly increased (P < 0.05), and the mRNA expression of PI3K and Akt was up-regulated obviously, while FKN mRNA expression was significantly decreased in diazoxide pretreatment group (P < 0.01). Diazoxide pretreatment+5-hydroxydecanoate group called off diazoxide pretreatment-induced changes, and did not differ from the hypoxia-reoxygenation group. These findings suggest that diazoxide pretreatment can promote cell proliferation and up-regulate the mRNA expression of PI3K and Akt as well as decrease FKN mRNA expression protect rat MMECs from hypoxia-reoxygenation.

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