Abstract: Objective To investigate the role of PI3K/Akt signal pathway in openned mito-KATP inhibit the expression of fractalkine (FKN) in rat myocardium microvascular endothelial cells exposed to hypoxia-reoxygenation. Methods Cardiac microvascular endothelial cells of the SD rat were cultured to establish a hypoxia-reoxygenation model. Twenty-four dishes were randomly divided into 4 groups ( EM>n/EM>=6 each).The normal control group (group N ), the cells of H/R group, diazoxide pretreatment +H/R group (group DZ) and diazoxide pretreatment+LY294002+ H/R group (group DZ+LY294002). BR>The cell vitality, the cell apoptotic rate and expression of Akt, FKN mRNA were detected with MTT. Hoechst dyeing RT-PCR and Western blotting, respectively. Results Compared with group N, the cell vitality significantly decreased ( EM>P /EM><0.01) and the apoptosis rate increased( EM>P/EM> <0.01). The expression of FKN mRNA and protein ( EM>P/EM> <0.01) was up-regulated in H/R group, the expression of Akt mRNA and protein significantly rised ( EM>P /EM><0.05).Compared with group H/R, the cell vitality significantly increased ( EM>P/EM> <0.05), the apoptosis rate significantly decreased (EM>P/EM><0.01).The expression of Akt mRNA and protein( EM>P/EM> <0.01and P <0.05) was up-regulated,fractalkine mRNA and significantly decreased ( EM>P/EM> <0.01) in group DZ. Compared with group DZ, Akt protein and mRNA significantly decreased (EM> P/EM> <0.01), BR>FKN mRNA and protein significantly increased ( EM>P /EM><0.01). Conclusion Openned mito-KATP through the PI3K/Akt signal pathway may regulate downstream of the transcription and expression of fractalkine mRNA inhibit cell apoptosis and improve the proliferation rate to protect the rat cardiac microvascular endothelial cells exposed on hypoxia-reoxygenation. BR

Key words: mito-KATP, Cardiac microvascular endothelial cell, PI3K, Akt, FKN, Hypoxia-reoxygenation, RT-PCR, Western blotting, Rat