We analyzed the potency of vicenin-2, flavanoid present in medicinal herbs such Ocimum sanctum and Moringa oleifera on inhibiting the STAT3 gene expression and its subsequent regulatory genes. We assessed the effect of vicenin-2 against the STAT-3 activation both in the normal and induced stage with IL-6 and EGF. To prove vicenin-2 as a ideal inhibitor of vicenin-2, the STAT3 regulated proteins, protein kinases and phosphatases were also analyzed. The anticancer effect of vicenin-2 was assessed with three different hepatocellular carcinoma cell lines and their effect of induction of apoptosis was assessed with immunoblotting analysis. To confirm the anticancer effect of vicenin-2, the xenografted hepatocellular mice model was treated with vicenin-2 and analyzed for tumor size reduction and apoptotic induction. Vicenin-2 significantly inhibited the STAT3 protein expression even in the presence of IL-6 and EGF induction. Vicenin-2 pretreated cells shown increased phosphorylation of STAT3 protein when treated with pervandate and SHP1-siRNA respectively. Vicenin-2 treatment decreased the expression of STAT3 regulated protein JAK1, JAK2, AKT and also increased the apoptotic proteins procaspase3, PARP. It significantly decreased the levels of antiapoptotic proteins Bcl2, Bclxl, Mcl1, survivig, cell regulatory protein cyclinD1 and angiogenic protein VEGF. In vivo results prove that vicenin-2 potentially inhibits the growth of tumour and induces apoptosis in xenografted hepatocellular mice model. Overall our in vitro and in vivo findings authentically prove that vicenin-2 is a novel STAT-3 inhibitor which imparts anticarcinogenic effect by inhibiting the STAT-3 signaling pathway.

我们分析了在圣药（Ocimum Sanctum）和辣木（Moringa oleifera）等药草中存在的总黄酮2（Vistanin-2）的功效抑制STAT3基因表达及其随后的调控基因。我们在正常和诱导期用IL-6和EGF评估了Vicenin-2对STAT-3激活的作用。为了证明Vic​​enin-2是Vicenin-2的理想抑制剂，还分析了STAT3调节的蛋白，蛋白激酶和磷酸酶。用三种不同的肝癌细胞系评估了Vicenin-2的抗癌作用，并通过免疫印迹分析评估了它们诱导凋亡的作用。为了确认Visinin-2的抗癌作用，用Visinin-2处理异种移植肝细胞小鼠模型，并分析其肿瘤大小的减少和凋亡的诱导。Vicenin-2甚至在存在IL-6和EGF诱导的情况下也显着抑制STAT3蛋白的表达。Vicenin-2预处理的细胞分别用过碘酸盐和SHP1-siRNA处理后，STAT3蛋白的磷酸化增强。Vicenin-2处理可降低STAT3调控蛋白JAK1，JAK2，AKT的表达，并增加凋亡蛋白procaspase3，PARP。它显着降低了抗凋亡蛋白Bcl2，Bclx1，Mcl1，survivig，细胞调节蛋白cyclinD1和血管生成蛋白VEGF的水平。体内结果证明，Visinin-2可能抑制异种移植肝细胞小鼠模型中的肿瘤生长并诱导细胞凋亡。总的来说，我们在体内和体外的发现可靠地证明了Vicenin-2是一种新型STAT-3抑制剂，可通过抑制STAT-3信号传导途径来赋予抗癌作用。