Department of Normal Surgical,, Xiangyang Central Hospital, Hubei University of Arts and Science, Xiangyang, Hubei 441053, P.R. China.
Department of Oncology, Xiangyang Central Hospital, Hubei University of Arts and Science, Xiangyang, Hubei 441053, P.R. China.
Mol Med Rep. 2017 Dec;16(6):8977-8982. doi: 10.3892/mmr.2017.7696. Epub 2017 Oct 3.
Bakuchiol is extracted from Psoralea corylifolia, a member of the Leguminosae family, has been used in Indian Ayurvedic and Chinese traditional medicine, and it possesses an anticancer effect. The primary aim of the present study was to identify the molecular mechanisms underlying the anticancer effect of bakuchiol monoterpenes. Bakuchiol treatment significantly inhibited NUGC3 human gastric cancer cell viability in a concentration dependent manner. In addition, bakuchiol significantly increased the apoptotic cell population in the sub‑G1 phase, and Annexin‑V‑fluorescein isothiocyanate/propidium iodide double staining confirmed the increase in apoptosis. Nuclear fragmentation and the formation of apoptotic organelles were promoted in bakuchiol‑treated NUGC3 cells. Western blotting results indicated that bakuchiol treatment significantly decreased procaspase‑3,6,8,9 and poly (ADP‑ribose) polymerase (PARP) expression levels, increased cleaved caspase‑3 and cleaved PARP expression levels, and increased the B cell lymphoma‑2 associated X, apoptosis regulator:B cell lymphoma‑extra large ratio. Bakuchiol‑treated NUGC3 cells demonstrated significantly reduced phosphorylated (p‑) protein kinase B (AKT) protein expression levels and elevated p‑extracellular signal related kinase 1/2 (ERK1/2), p‑c‑Jun N‑terminal kinase (JNK) and p‑p38. Bakuchiol‑induced cell death was mitochondrial dependent, through modulation of phosphoinositide 3‑kinase/AKT and mitogen‑activated protein kinase signaling pathways. These findings demonstrated that bakuchiol possesses potential for treating human gastric cancer.
补骨脂素是从豆科补骨脂属植物中提取的,具有抗癌作用,已在印度阿育吠陀和中国传统医学中使用。本研究的主要目的是鉴定补骨脂素单萜的抗癌作用的分子机制。补骨脂素处理以浓度依赖性方式显著抑制 NUGC3 人胃癌细胞活力。此外,补骨脂素显著增加了亚 G1 期的凋亡细胞群体,并且 Annexin-V-异硫氰酸荧光素/碘化丙啶双重染色证实了凋亡的增加。核片段化和凋亡细胞器的形成在补骨脂素处理的 NUGC3 细胞中得到促进。Western blot 结果表明,补骨脂素处理显著降低了 procaspase-3、6、8、9 和多聚(ADP-核糖)聚合酶(PARP)的表达水平,增加了 cleaved caspase-3 和 cleaved PARP 的表达水平,并增加了 B 细胞淋巴瘤-2 相关 X,凋亡调节因子:B 细胞淋巴瘤-extra large 比值。补骨脂素处理的 NUGC3 细胞表现出显著降低的磷酸化(p)蛋白激酶 B(AKT)蛋白表达水平和升高的 p-细胞外信号相关激酶 1/2(ERK1/2),p-c-Jun N-末端激酶(JNK)和 p-p38。补骨脂素诱导的细胞死亡是线粒体依赖性的,通过调节磷酸肌醇 3-激酶/AKT 和丝裂原活化蛋白激酶信号通路。这些发现表明补骨脂素具有治疗人类胃癌的潜力。