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目的:探讨褪黑素(MLT)对体外培养的肺腺癌A549细胞增殖的影响及作用机制。方法:体外培养人肺腺癌A549细胞,通过不同浓度的褪黑素(0.1、1.0、2.5、5.0mmol/L)干预24、48、72h,通过噻唑蓝(MTT)法测定细胞增殖,DNA末端原位标记染色法(Tunel)检测细胞凋亡情况,蛋白印迹(Western-blot)法检测褪黑素对A549细胞核内核转录因子Bp65(NF-Bp65)蛋白水平的影响。结果:褪黑素能够抑制人肺腺癌A549细胞增殖,呈剂量、时间依赖性性;高浓度褪黑素作用后凋亡细胞比例明显升高,同时细胞核内NF-Bp65蛋白量明显减少。结论:褪黑素能够呈剂量、时间依赖性抑制人肺腺癌A549细胞的增殖,抑制核因子Bp65的核移位诱导细胞凋亡是可能作用路径之一。
Objective: To investigate the effect of melatonin (MLT) on the proliferation of human lung adenocarcinoma A549 cells and its mechanism. Methods: Human lung adenocarcinoma A549 cells were cultured in vitro. The cells were exposed to various concentrations of melatonin (0.1, 1.0, 2.5 and 5.0 mmol / L) for 24, 48 and 72 hours. Cell proliferation, DNA end The apoptosis of A549 cells was detected by Tunel, and the effect of melatonin on the expression of nuclear factor Bp65 (NF-Bp65) in A549 cells was detected by Western-blot. Results: Melatonin could inhibit the proliferation of human lung adenocarcinoma A549 cells in a dose-and time-dependent manner. The proportion of apoptotic cells increased significantly after treated with high concentration of melatonin, and the amount of NF-Bp65 protein in the nucleus decreased significantly. CONCLUSION: Melatonin can inhibit the proliferation of human lung adenocarcinoma A549 cells in a dose-dependent and time-dependent manner. Inhibition of nuclear translocation of nuclear factor Bp65 induces apoptosis is one of the possible pathways.