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本研究探讨不同浓度的油茶籽壳乙酸乙酯提取物对Hep G2细胞的增殖抑制作用,及其诱导细胞凋亡的机制。以油茶籽壳乙酸乙酯提取物为原材料,以Hep G2细胞为研究对象,采用CCK-8法测定油茶籽壳乙酸乙酯提取物对Hep G2细胞的抗增殖作用;采用流式细胞术和荧光定量PCR分别检测油茶籽壳乙酸乙酯提取物对Hep G2细胞的周期阻滞情况及相关凋亡基因(Survivn,Bcl-2,Bax和caspase-3)的表达水平。结果表明:油茶籽壳乙酸乙酯提取物对Hep G2细胞具有显著的增殖抑制作用,且在一定浓度范围内62.5~250μg/m L具有剂量依耐性;Hep G2细胞经一定浓度提取物50μg/m L、100μg/m L、200μg/m L诱导处理24 h后,发生G_0/G_1期阻滞,且使Survivin及Bcl-2的表达降低,Caspase-3及Bax的表达上升,导致细胞发生凋亡。
This study was aimed to investigate the effects of different concentrations of ethyl acetate extracts from Camellia oleifera seeds on proliferation of Hep G2 cells and its mechanism of apoptosis. Using the ethyl acetate extract of Camellia oleifera seed shell as the raw material, Hep G2 cells were used as the research object. The anti-proliferative effects of ethyl acetate extracts of Camellia oleifera seeds on Hep G2 cells were determined by CCK-8 method. Flow cytometry and fluorescence Quantitative PCR was used to detect the cycle arrest of Hep G2 cells and the expression of related apoptosis genes (Survivn, Bcl-2, Bax and caspase-3) of ethyl acetate extract from Camellia oleifera seed shell. The results showed that the ethyl acetate extract of Camellia oleifera seed shell could inhibit the proliferation of Hep G2 cells in a dose-dependent manner at a dose range of 62.5 ~ 250μg / m L; Hep G2 cells were treated with 50μg / m L, 100μg / ml, 200μg / ml L for 24 h, G0 / G1 phase arrest occurred, and the expression of Survivin and Bcl-2 decreased, and the expression of Caspase-3 and Bax increased, leading to cell apoptosis .