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本研究的目的在于研究不同浓度和厚朴酚对人肺癌A2细胞增殖和凋亡的影响,分析凋亡的可能机制。通过台盼蓝拒染法检测和厚朴酚对细胞增殖的影响,荧光显微镜下观察细胞形态的变化,流式细胞术检测细胞凋亡率和细胞周期的变化,qRT-PCR和Western blotting分别检测Bax、Bcl-2基因mRNA和蛋白表达情况。结果表明,在一定范围内,和厚朴酚对人肺癌A2细胞增殖有抑制作用且呈时间和剂量依赖性,其作用人肺癌A2细胞24 h、48 h和72 h的IC50值分别为44.03 nmol/L、26.51 nmol/L和19.54 nmol/L。不同浓度的和厚朴酚作用人肺癌A2细胞48 h后,细胞出现明显的凋亡特征,早期凋亡细胞增多,且G1期和G2期细胞减少,S期细胞增多。与对照组相比,Bax mRNA和蛋白表达均显著升高(p<0.05),Bcl-2mRNA和蛋白表达均显著降低(p<0.05)。本研究表明一定浓度范围的和厚朴酚能抑制人肺癌A2细胞增殖,诱导细胞凋亡且呈时间和剂量依赖性,并可上调Bax基因表达,下调Bc L-2基因表达。
The purpose of this study was to investigate the effects of different concentrations of honokiol on the proliferation and apoptosis of human lung cancer A2 cells, and to analyze the possible mechanism of apoptosis. The effects of honokiol on cell proliferation were detected by trypan blue exclusion method. The morphological changes of cells were observed under a fluorescence microscope. The apoptosis rate and cell cycle were detected by flow cytometry. The expression of honokiol was detected by qRT-PCR and Western blotting Bax, Bcl-2 mRNA and protein expression. The results showed that, within a certain range, honokiol inhibited the proliferation of human lung cancer A2 cells in a time and dose-dependent manner, and the IC50 values of human lung adenocarcinoma A2 cells at 24 h, 48 h and 72 h were 44.03 nmol /L, 26.51 nmol / L and 19.54 nmol / L. After being treated with different concentrations of honokiol for 48 hours, the cells showed obvious apoptotic features. The number of early apoptotic cells increased, and the number of cells in G1 and G2 phase decreased and the number of S phase cells increased. Compared with the control group, Bax mRNA and protein expression were significantly increased (p <0.05), Bcl-2 mRNA and protein expression were significantly reduced (p <0.05). The present study shows that honokiol can inhibit the proliferation and induce apoptosis of human lung adenocarcinoma A2 cells in a dose and time-dependent manner, and can up-regulate Bax gene expression and down-regulate Bcl-2 gene expression.