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目的:探讨不同剂量阿司匹林对大鼠心肌微血管内皮细胞(CMECs)血管新生功能的影响和可能的机制。方法:消化法分离大鼠CMECs,用不同浓度(1、10、100、1 000和5 000μmol/L)的阿司匹林处理体外培养的大鼠CMECs后,分别用CCK-8比色法检测细胞增殖、TUNEL法检测细胞凋亡、划痕试验及Transwell小室评价细胞迁移能力、成管实验评价血管新生能力、Western blot法检测蛋白激酶B(AKT)磷酸化水平,ELISA法测定纤维连接蛋白(FN)表达。结果:11、10和100μmol/L的阿司匹林对,CMECs的增殖、凋亡和AKT磷酸化水平无明显影响,1 000、5 000μmol/L的阿司匹林对组显著抑制CMECs增殖、下调AKT磷酸化水平、诱导细胞凋亡;210、100μmol/L的阿司匹林促进CMECs迁移、成管;3FN表达随阿司匹林浓度升高而升高。结论:1低浓度阿司匹林(1~100μmol/L)对CMECs的存活无明显影响,而高浓度的阿司匹林(1 000、5 000μmol/L)显著抑制CMECs增殖、下调AKT磷酸化水平、细胞凋亡增多。2低浓度阿司匹林(1~100μmol/L)作用下,阿司匹林促进CMECs迁移、成管能力,可能与阿司匹林作为环氧化酶(COX)抑制剂,减少前列环素(PGI2)生成引起FN表达上调有关。
Objective: To investigate the effects of different doses of aspirin on angiogenesis in rat cardiac microvascular endothelial cells (CMECs) and its possible mechanism. METHODS: Rat CMECs were isolated by digestion and treated with different concentrations of aspirin (1, 10, 100, 1000 and 5000 μmol / L). The proliferation of CMECs were detected by CCK-8 colorimetric assay. TUNEL assay was used to detect apoptosis, scratch test and cell migration assay in Transwell chamber. The ability of angiogenesis was evaluated by tube formation assay. Protein kinase B (AKT) phosphorylation was detected by Western blot and fibronectin (FN) by ELISA . RESULTS: Aspirin at 11, 10 and 100 μmol / L had no significant effect on the proliferation, apoptosis and AKT phosphorylation of CMECs. Aspirin at 1 000 and 5 000 μmol / L significantly inhibited the proliferation of CMECs and down-regulated the phosphorylation of AKT, Induced apoptosis; 210,100μmol / L aspirin promoted the migration of CMECs into tube; 3FN expression increased with the increase of aspirin concentration. CONCLUSION: 1 low concentration aspirin (1 ~ 100μmol / L) has no significant effect on the survival of CMECs, while high concentration of aspirin (1000, 5000μmol / L) significantly inhibited the proliferation of CMECs, downregulated the phosphorylation of AKT, increased apoptosis . 2 Under the action of low concentration of aspirin (1 ~ 100μmol / L), aspirin can promote the migration and formation of CMECs, which may be related to the decrease of the production of PGI2 induced by aspirin as a cyclooxygenase (COX) inhibitor and PGI2 .