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目的探讨可溶性环氧化物水解酶抑制剂(s EHi)AUDA调控颈动脉狭窄(CS)患者外周血内皮祖细胞(EPCs)增殖的分子机制。方法从CS患者外周血分离、培养内皮祖细胞,收集培养至第7 d的细胞,分为未处理组、AUDA组、PI3K抑制剂(LY294002)组和AUDA+LY294002组,取无颈动脉狭窄患者的EPCs作为对照组,MTT法检测EPCs的增殖能力,Western blot法检测EPCs Akt磷酸化的水平。结果对照组EPCs增殖能力较未处理组增强,AUDA组较未处理组、AUDA+LY294002组、LY294002组EPCs增殖能力增强,未处理组、AUDA+LY294002组较LY294002组内皮祖细胞增殖能力增强;Western blot结果显示AUDA可以促进EPCs P-Akt蛋白的表达,而LY294002可以抑制上述作用。结论 AUDA可能通过活化PI3K/Akt信号通路来促进内皮祖细胞的增殖。
Objective To investigate the molecular mechanism of soluble epoxide hydrolase inhibitor (s EHi) AUDA in the proliferation of peripheral endothelial progenitor cells (EPCs) in patients with carotid artery stenosis (CS). Methods Peripheral blood progenitor cells were isolated from peripheral blood of CS patients and cultured on the 7th day. The cells were collected and were divided into untreated group, AUDA group, PI3K inhibitor (LY294002) group and AUDA + LY294002 group. The patients without carotid artery stenosis EPCs were used as control group. The proliferation of EPCs was detected by MTT assay. The phosphorylation of Akt in EPCs was detected by Western blot. Results The proliferation of EPCs in control group was enhanced compared with that in untreated group. The proliferation of EPCs in AUDA group, AUDA + LY294002 group and LY294002 group was enhanced. In untreated group, the proliferation of EPCs in AUDA + LY294002 group was stronger than that in LY294002 group. blot results showed that AUDA can promote the expression of EPCs P-Akt protein, and LY294002 can inhibit the above effects. Conclusion AUDA may promote the proliferation of endothelial progenitor cells by activating the PI3K / Akt signaling pathway.