CAJ | 학술논문

目的：探讨吗啡联合顺铂处理肺癌A549细胞后，细胞增殖能力和细胞凋亡水平的变化。方法：选择不同浓度吗啡处理肺癌A549细胞，CCK8法检测6、12、24和48 h时点的细胞增殖抑制率；再采用30μg/mL顺铂单药联合筛选出的最佳抑制率浓度的吗啡处理细胞，48 h后检测细胞增殖活力，同时采用Western blot电泳检测顺铂单药、吗啡，以及二者联合分别处理细胞后，凋亡相关蛋白Bax、Bcl-2、Caspase-3、survivin表达量的变化。结果：CCK8法显示500μg/mL浓度的吗啡单独处理肺癌细胞48 h时，能最明显抑制细胞的增殖（P＜0.05），抑制率达到41.2%；与单纯使用顺铂抑制细胞增殖效果（47.21%）相比，顺铂30μg/mL联合500μg/mL吗啡对细胞的抑制率达77.45%，差异具有统计学意义（P＜0.05）；Western blot实验显示顺铂联合500μg/mL吗啡与单纯顺铂药物作用相比，Bcl-2、survivin蛋白表达量降低，Bax、Caspase-3蛋白的表达升高。结论：选择合适的吗啡浓度可加强顺铂对肺癌细胞的抑制增殖和促凋亡功能，这种对肺癌细胞的生物学效应可能与促进凋亡蛋白Bax、Caspase-3表达上调和凋亡抑制蛋白的下调相关。
목적：탐토마배연합순박처리폐암A549세포후，세포증식능력화세포조망수평적변화。방법：선택불동농도마배처리폐암A549세포，CCK8법검측6、12、24화48 h시점적세포증식억제솔；재채용30μg/mL순박단약연합사선출적최가억제솔농도적마배처리세포，48 h후검측세포증식활력，동시채용Western blot전영검측순박단약、마배，이급이자연합분별처리세포후，조망상관단백Bax、Bcl-2、Caspase-3、survivin표체량적변화。결과：CCK8법현시500μg/mL농도적마배단독처리폐암세포48 h시，능최명현억제세포적증식（P＜0.05），억제솔체도41.2%；여단순사용순박억제세포증식효과（47.21%）상비，순박30μg/mL연합500μg/mL마배대세포적억제솔체77.45%，차이구유통계학의의（P＜0.05）；Western blot실험현시순박연합500μg/mL마배여단순순박약물작용상비，Bcl-2、survivin단백표체량강저，Bax、Caspase-3단백적표체승고。결론：선택합괄적마배농도가가강순박대폐암세포적억제증식화촉조망공능，저충대폐암세포적생물학효응가능여촉진조망단백Bax、Caspase-3표체상조화조망억제단백적하조상관。
Objective:To analyze the effect and mechanism of the proliferation inhibition and apoptosis in human lung carcinoma after using morphine combined with cisplatin chemotherapy. Methods:Human lung ad-enocarcinoma cell line A549 was cultured in conventional 1 640 medium. Cell proliferation activity for cisplatin alone or in combination with morphine after treatment for 6 h, 12 h, 24 h and 48 h were detected by CCK8. In addition, Western Blot electrophoresis was adopted to detect cisplatin alone or in combination with the optimal concentration of morphine after 48 h. Then changes of apoptosis related proteins Bax, Bcl-2 Caspase-3, survivin expression level were analyzed. Results:After 24 h, or 48 h, the concentration of 500μg/mL morphine in combi-nation with cisplatin group, compared to morphine and cisplatin alone group, could signiifcantly increase cancer cell proliferation inhibitory effect (P<0.05). While combined with low-dose concentrations of morphine-treated group, compared with cisplatin alone, the difference was not statistically signiifcant. By WB experiments, we found that the combination of drug treatment could inhibit Bcl-2, survivin protein expression induced by cisplat-in, while enhancing the pro-apoptosis death proteins Bax, Caspase-3 expression. Conclusion:The best choice for morphine dosage can signiifcantly enhance proliferation and apoptosis function of cisplatin on lung cancer cell. This may inhibit the proliferation of lung cancer cells by promoting key apoptotic protein Bax and Caspase-3 ex-pression pathway.