目的 探討卡培他濱聯(lián)合阿司匹林對SGC-7901細胞增殖和凋亡的體外抑制作用及其作用機制。方法 體外培養(yǎng)SGC-7901細胞，MTT法檢測卡培他濱1.0 μmol/L與阿司匹林0.5、1.0、3.0 mmol/L單用和聯(lián)用對SGC-7901細胞體外增殖的抑制作用；倒置相差顯微鏡觀察卡培他濱1.0 μmol/L與阿司匹林3.0 mmol/L單獨及聯(lián)合用藥對SGC-7901細胞形態(tài)的影響；PI/Annexin V-FITC雙染色流式細胞術(shù)分析卡培他濱1.0 μmol/L與阿司匹林3.0 mmol/L單獨及聯(lián)合用藥誘導SGC-7901的細胞凋亡率；Western blotting分析卡培他濱1.0 mmol/L與阿司匹林3.0 mmol/L單獨及聯(lián)合用藥對COX-2、VEGF表達的影響。結(jié)果 卡培他濱與阿司匹林對SGC-7901細胞均有生長抑制作用，且聯(lián)合組的抑制率高于卡培他濱組和阿司匹林組，兩組間比較差異具有統(tǒng)計學意義（P<0.05）。用藥處理24 h后，在顯微鏡下可觀察到SGC-7901細胞發(fā)生細胞凋亡的形態(tài)學改變，聯(lián)合組相對于卡培他濱、阿司匹林單獨用藥組的變化更明顯。PI/Annexin V雙染分析表明，卡培他濱1.0 μmol/L＋阿司匹林3.0 mmol/L聯(lián)合組的細胞凋亡率明顯高于阿司匹林3.0 mmol/L組或卡培他濱1.0 μmol/L組。阿司匹林3.0 mmol/L、卡培他濱1 μmol/L以及卡培他濱1.0 μmol/L＋阿司匹林3.0 mmol/L聯(lián)合組電泳可以檢測出環(huán)氧合酶-2（COX-2）、血管內(nèi)皮生長因子（VEGF）的特異蛋白條帶。阿司匹林單用時，COX-2表達量受到抑制（P<0.01），蛋白表達下調(diào)，而VEGF表達無明顯抑制；卡培他濱單用時，VEGF表達量受到抑制（P<0.01），蛋白表達下調(diào)，而COX-2表達無明顯抑制；卡培他濱聯(lián)合阿司匹林處理時，SGC-7901細胞的COX-2、VEGF表達量均受到抑制（P<0.01），同時下調(diào)COX-2及VEGF蛋白表達。結(jié)論 卡培他濱聯(lián)合阿司匹林能夠明顯抑制胃癌SGC-7901細胞的增殖，并促進其凋亡，其作用機制與COX-2、VEGF蛋白表達的調(diào)控有關(guān)。

Objective To investigate inhibitory effect of capecitabine combine with aspirin on proliferation of SGC 7901 cell in vitro and its mechanisms. Methods SGC-7901 cells were cultured in vitro. Inhibitory rates of capecitabine (1.0 μmol/L) or/and aspirin (0.5, 1.0, and 3.0 mmol/L) on SGC 7901 cell were detected by MTT method. The morphological changes of SGC-7901 cells treated by capecitabine (1.0 μmol/L) and aspirin (3.0 mmol/L) alone or in combination were observed by fluorescence microscopy. Apoptosis rates of SGC-7901 cells treated by capecitabine (1.0 μmol/L) and aspirin (3.0 mmol/L) alone or in combination were determined by Annexin VFIT C/PI kit and flow cytometry. The expressions of COX-2 and VEGF treated by capecitabine (1.0 μmol/L) and aspirin (3.0 mmol/L) alone or in combination were determined by Western blotting method. Results Capecitabine and aspirin all had inhibitory effects on growth of SGC-7901 cells, and the inhibition rates of combined group were higher than those in capecitabine group and aspirin group, with significant difference between two groups (P<0.05). Morphological changes of SGC-7901 cells were observed under microscope after treatment for 24 h, and changes in the combined group were more obvious than those in capecitabine group and aspirin group. Flow cytometry showed that apoptosis rates in the capecitabine (1.0 μmol/L)+aspirin (3.0 mmol/L) group was significantly higher than that of capecitabine (1.0 μmol/L) group or aspirin (3.0 mmol/L) group. The specific protein bands of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) in capecitabine (1.0 μmol/L) and aspirin (3.0 mmol/L) alone or in combination group could be detected by electrophoresis. When SGC-7901 cells were treated by aspirin alone, the expression of COX-2 was inhibited (P<0.01), and protein expression was down-regulated, but the expression of VEGF was not inhibited. While SGC-7901 cells were treated by capecitabine alone, the expression of VEGF was inhibited (P<0.01), and protein expression was down-regulated, but the expression of COX-2 was not inhibited. COX-2 and VEGF expression were inhibited when treated by capecitabine combined with aspirin (P<0.01), and the expression of COX-2 and VEGF protein were down-regulated. Conclusion Capecitabine combined with aspirin can significantly inhibit proliferation of SGC-7901 cell, and induce apoptosis, and its mechanism may be related to the regulation of COX-2 and VEGF protein expression.