Delphinidin is an anthocyanin that belongs to the group of flavonoids that exert numerous biological activities. However, the molecular mechanisms underlying the anticancer effects of delphinidin remain poorly understood. In our study we analyzed delphinidin modulate STAT-3 and MAPKinase signaling thereby inhbits cell proliferation and promote apoptosis. Our study demonstrated that delphinidin treatment significantly reduced the viability of human colon cancer HCT116 in a concentration-dependent manner. We noticed that delphinidin effectively induced oxidative stress-mediated apoptosis by generating intracellular ROS, decreasing antioxidant levels, inducing lipid peroxidation, and single-strand break on colon cancer cells. In this study, we observed that delphinidin treatment alters the mitochondrial membrane potential, thereby induces apoptosis was closely associated with the induction of pro-apoptotic Bax, Caspase- 3,8 & 9, cytochrome C, and inhibition of anti-apoptotic protein expression. Studies on STAT-3 and MAPKinase signaling showed delphinidin inhibited the phosphorylation of these transcription factors' activity. Inhibition of STAT-3, p38, and ERK1/2 phosphorylation and modulation pro-apoptotic protein expression might be responsible for the anticancer activity of delphinidin in colon cancer cells.

中文翻译：

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Delphinidin 调节 JAK/STAT3 和 MAPKinase 信号传导以诱导 HCT116 细胞凋亡

Delphinidin 是一种花青素，属于具有多种生物活性的黄酮类化合物。然而，飞燕草素抗癌作用的分子机制仍然知之甚少。在我们的研究中，我们分析了飞燕草素调节 STAT-3 和 MAPKinase 信号传导从而抑制细胞增殖并促进细胞凋亡。我们的研究表明，飞燕草素治疗以浓度依赖性方式显着降低了人结肠癌 HCT116 的活力。我们注意到飞燕草素通过产生细胞内 ROS、降低抗氧化水平、诱导脂质过氧化和结肠癌细胞的单链断裂来有效诱导氧化应激介导的细胞凋亡。在这项研究中，我们观察到飞燕草素处理会改变线粒体膜电位，从而诱导细胞凋亡与促凋亡 Bax、Caspase-3,8 和 9、细胞色素 C 的诱导以及抗凋亡蛋白表达的抑制密切相关。对 STAT-3 和 MAPKinase 信号传导的研究表明，翠雀素可抑制这些转录因子活性的磷酸化。抑制 STAT-3、p38 和 ERK1/2 磷酸化并调节促凋亡蛋白表达可能是飞燕草素在结肠癌细胞中的抗癌活性的原因。