Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Department of Experimental Therapeutics, The University of Texas MD Anderson Cancer Center, Houston, TX, 77030, USA.
Phytomedicine. 2017 Oct 15;34:171-181. doi: 10.1016/j.phymed.2017.08.021. Epub 2017 Aug 31.
While the anti-inflammatory and anticancer potential of curcumin, which is derived from turmeric (Curcuma longa), has been studied extensively, very little is known about Calebin A, another novel compound from the same source.
To determine whether Calebin A exhibits anti-inflammatory and anticancer potential.
We examined the anti-inflammatory potential of Calebin A by DNA binding of NF-κB. Anticancer properties of Calebin were determined by MTT and FACS analysis and NF-κB regulated expression of proteins was assessed by western blotting.
Calebin A suppressed NF-κB activation induced by various stimuli. This inhibition of NF-κB activation was mediated through the suppression of direct binding of NF-κB/p65 to the DNA. This inhibitory effect was reversed by a reducing agent, and mutation of the Cys38 of p65 to serine abolished the effect of Calebin A on this binding. Suppression of NF-κB activation by Calebin A resulted in the down-regulation of the expression of proteins involved in tumor cell survival, proliferation, inflammation, and metastasis. Furthermore, Calebin A inhibited proliferation and induced apoptosis in a wide variety of tumor cells, as examined by various assays. It enhanced apoptosis induced by chemotherapeutic agents.
Our results demonstrate that Calebin A inhibits NF-κB activation pathway through interaction with p65 and potentiates apoptosis in cancer cells; thus, it has potential in the treatment of cancer. However, further in vivo studies are warranted to define its anti-inflammatory and anticancer potential.
姜黄（Curcuma longa）中提取的姜黄素具有抗炎和抗癌潜力，已得到广泛研究，而其来源的另一种新型化合物 Calebin A 则知之甚少。
确定 Calebin A 是否具有抗炎和抗癌潜力。
我们通过 NF-κB 的 DNA 结合来研究 Calebin A 的抗炎潜力。通过 MTT 和 FACS 分析来确定 Calebin 的抗癌特性，并通过 Western blot 评估 NF-κB 调控的蛋白表达。
Calebin A 抑制了各种刺激诱导的 NF-κB 激活。这种 NF-κB 激活的抑制是通过抑制 NF-κB/p65 与 DNA 的直接结合来介导的。还原剂可逆转这种抑制作用，而将 p65 的 Cys38 突变为丝氨酸则可消除 Calebin A 对这种结合的作用。Calebin A 抑制 NF-κB 激活导致参与肿瘤细胞存活、增殖、炎症和转移的蛋白表达下调。此外，通过各种测定，Calebin A 抑制了多种肿瘤细胞的增殖并诱导了细胞凋亡。它增强了化疗药物诱导的细胞凋亡。
我们的研究结果表明，Calebin A 通过与 p65 相互作用抑制 NF-κB 激活途径，并增强癌细胞凋亡；因此，它具有治疗癌症的潜力。然而，需要进一步的体内研究来确定其抗炎和抗癌潜力。
