Liang Hua, Gu Miao-Ning, Yang Cheng-Xiang, Wang Han-Bing, Wen Xian-Jie, Zhou Qiao-Ling
Department of Anesthesiology, Southern Medical University, Guangzhou China.
Asian Pac J Cancer Prev. 2011;12(12):3415-20.
PURPOSE: Sevoflurane, an inhalational anesthetic, is used extensively during lung cancer surgery. However, the effect of sevoflurane on growth of lung carcinoma cells remains unclear. The purpose of this study is to investigate effects on proliferation, apoptosis, and cell cycling in the A549 human lung adenocarcinoma cell line. METHODS: A549 cells were treated with 1.7%, 3.4%, and 5.1 % sevoflurane for 2, 4, and 6 hours. Cell proliferation was evaluated by the MTT assay and colony formation assay. Apoptosis and cell cycle was analyzed by flow cytometry. Expression of X-linked inhibitor of apoptosis protein (XIAP), survivin, Bcl-2, Bax, caspase-3, cyclin A, cyclin B1, and cdc2 was measured by Western blotting. RESULTS: Significant inhibition of cell proliferation and induction of apoptosis were found in A549 cells after sevoflurane treatment. Simultaneously, expression of XIAP and survivin was supressed, while that of caspase-3 increased significantly, but Bcl-2 and Bax were not altered. Sevoflurane caused cell cycle arrest at the G2/M phase. At the same time, data revealed that cyclin A, cyclin B1, and cdc2 expression was down-regulated after sevoflurane treatment. CONCLUSION: This study demonstrated that sevoflurane inhibited proliferation, and induced apoptosis in human lung adenocarcinoma A549 cells, associated with down-regulated expression of XIAP and suvivin, and activating caspase-3.
目的:七氟醚作为一种吸入性麻醉剂,在肺癌手术中被广泛使用。然而,七氟醚对肺癌细胞生长的影响仍不清楚。本研究的目的是探讨其对A549人肺腺癌细胞系增殖、凋亡和细胞周期的影响。 方法:将A549细胞分别用1.7%、3.4%和5.1%的七氟醚处理2、4和6小时。通过MTT法和集落形成试验评估细胞增殖。通过流式细胞术分析凋亡和细胞周期。通过蛋白质印迹法检测凋亡蛋白X连锁抑制剂(XIAP)、生存素、Bcl-2、Bax、半胱天冬酶-3、细胞周期蛋白A、细胞周期蛋白B1和细胞周期蛋白依赖性激酶2(cdc2)的表达。 结果:七氟醚处理后,A549细胞的细胞增殖受到显著抑制,凋亡被诱导。同时,XIAP和生存素的表达受到抑制,而半胱天冬酶-3的表达显著增加,但Bcl-2和Bax未发生改变。七氟醚导致细胞周期阻滞在G2/M期。同时,数据显示七氟醚处理后细胞周期蛋白A、细胞周期蛋白B1和cdc2的表达下调。 结论:本研究表明,七氟醚抑制人肺腺癌A549细胞的增殖并诱导其凋亡,这与XIAP和生存素表达下调以及激活半胱天冬酶-3有关。
Asian Pac J Cancer Prev. 2011
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