在本篇研究中，藉由探討細胞增生（proliferation）、細胞週期（cell cycle）及細胞凋亡（apoptosis）等機制，評估蘆薈大黃素（aloe-emodin）對於人類前骨髓白血病細胞株（HL-60）抗癌的角色。由實驗數據發現，蘆薈大黃素對人類前骨髓白血病細胞株會抑制細胞增生、細胞週期停止在G2/M期(G2 / M phase arrest)及誘導細胞凋亡。同時由西方點墨法(immunobloting) 分析細胞週期素(cyclin A、cyclin B1及cyclin E)，結果顯示蘆薈大黃素對cyclin E無影響，而cyclin A、cyclin B1增加。分析細胞週期素激酶（CDK1及CDK2），CDK1增加而CDK2無影響。另一方面，而引發細胞週期停止在G2/M期之上游因子p27的表現量也會隨著加入蘆薈大黃素而表現量增加，故推論p27也許是調控促使人類前骨髓白血病細胞株發生細胞週期停止在G2/M期的主要因子。流式細胞儀分析實驗與DNA裂解實驗指出，蘆薈大黃素會誘發人類前骨髓白血病細胞株產生凋亡現象(apoptosis)；而且加入10 μM 蘆薈大黃素處理12、24、48與72小時之後，caspase-3的表現量增加。綜合以上之論點得之，蘆薈大黃素的抗癌活性在於抑制人類前骨髓白血病細胞株細胞增殖、引發細胞週期停止在G2/M期與活化caspase-3而促使凋亡發生。; In this study, we have evaluated the chemopreventive role of aloe-emodin in human promyelocytic leukemia (HL-60) cells in vitro by studying the regulation of proliferation, cell cycle and apoptosis. Aloe-emodin inhibited cell proliferation and induced G2/M arrest and apoptosis in HL-60 cells. Investigation on the levels of cyclins B1, E and A by immunoblot analysis showed that cyclin E level was unaffected, whereas cyclin B1 and A levels increased with increasing aloe-emodin in HL-60 cells. Investigation on the levels of cyclin-dependent kinases, Cdk1 and 2, showed that Cdk1 level was increased, where but Cdk2 level was not effected with aloe-emodin in HL-60 cells. The level of p27 was increased after HL-60 cells were cotreated with various concentrations of aloe-emodin. The increase of the levels of p27 may be the major factor for aloe-emodin to cause G2/M arrest in this examined cells. Flow cytometric assays and DNA fragmentation gel electrophoresis also confirmed that aloe-emodin induced apoptosis in HL-60 cells. The level of caspase-3 was increased after HL-60 cells were cotreated with 10 μM aloe-emodin for 12, 24, 48, and 72 hours. Taken together, aloe-emodin therefore appears to exert its anticarcinogenis properties by inhibiting proliferation and inducing cell cycle arrest and apoptosis underwent activation of caspase-3 in human leukemia HL-60 cells.
