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.rnOBJECTIVE: 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.rnMETHODS: 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.rnRESULTS 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.%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.
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