The present study examined the apoptotic effects and the underlying mechanism of sappanchalcone, a major bioactive compound isolated from Caesalpinia sappan L. on human colon cancer cells. To achieve this, we used two different colon cancer cell lines, namely HCT116 (as wild-type p53 cells) and SW480 (as p53-mutant cells) cells. Our results illustrated that sappanchalcone treatment decreased the proliferation and further promoted apoptosis in HCT116 cells compared with the findings in SW480 cells. Sappanchalcone triggered phosphorylation of p53, which is involved in the activation of caspases and increased expression of Bax in HCT116 cells. Conversely, sappanchalcone-treated SW480 cells displayed no change in p53 phosphorylation or caspase activation. In addition, sappanchalcone further increased reactive oxygen species (ROS) levels and apoptosis-inducing factor (AIF) release in both HCT116 and SW480 cells. These data suggest that sappanchalcone induces apoptosis through caspase-dependent and caspases-independent mechanisms that were characterized by decreased Bcl-2 expression, mitochondrial targeting, and altered ROS production and AIF translocation to the nuclei.

本研究检查了细胞凋亡作用和sappanchalcone的基本机制，一个主要的生物活性化合物分离自苏木L.在人结肠癌细胞上。为了实现这一目标，我们使用了两种不同的结肠癌细胞系，即HCT116（作为野生型p53细胞）和SW480（作为p53突变细胞）细胞。我们的结果表明，与SW480细胞相比，Sappanchalcone处理可降低HCT116细胞的增殖并进一步促进细胞凋亡。萨帕查酮触发了p53的磷酸化，这与caspase的活化和HCT116细胞中Bax的表达增加有关。相反，经桑帕查酮处理的SW480细胞在p53磷酸化或半胱天冬酶激活中未显示任何变化。此外，Sappanchalcone进一步增加了HCT116和SW480细胞中的活性氧（ROS）水平和凋亡诱导因子（AIF）释放。