■喉癌是一种头颈部肿瘤,预后和生存率较差。全球喉癌的新病例迅速增加,死亡率更高。
■目前的研究工作集中在揭示onononin对喉癌Hep-2细胞的体外抗肿瘤作用。
■使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四唑溴化物(MTT)测定法研究了ononin对喉癌Hep-2细胞和正常HuLa-PC喉细胞的细胞毒性作用。细胞内活性氧(ROS)的产生,凋亡性细胞死亡,线粒体膜电位(MMP),使用各自的染色测定法检测25和50µM的onononin处理的Hep-2细胞上的细胞粘附。使用特定试剂盒测定TBARS和抗氧化剂的水平。c-Jun氨基末端激酶1/2(JNK1/2)的表达,细胞外信号调节激酶1/2(ERK1/2),p38,磷脂酰肌醇-3激酶1/2(PI3K1/2),使用逆转录聚合酶链反应(RT-PCR)测定法研究了经onononin处理的Hep-2细胞中的蛋白激酶B(Akt)。
■onononin处理有效抑制Hep-2细胞活力,但不影响HuLa-PC细胞的活力。此外,有效改善了细胞内ROS的积累,耗尽了MMP,并引发Hep-2细胞凋亡。对硫代巴比妥酸活性物质(TBARS)进行了改进,和谷胱甘肽(GSH)的水平和超氧化物歧化酶(SOD)在服用甲素的Hep-2细胞中被耗尽。在Hep-2细胞中,ononin处理基本上抑制JNK/ERK/p38轴。
■一起,这项探索的结果证明了ononin对喉癌Hep-2细胞具有显着的抗肿瘤活性。
UNASSIGNED: Laryngeal cancer is a type of head and neck tumor with a poor prognosis and survival rate. The new cases of laryngeal cancer increased rapidly with a higher mortality rate around the world.
UNASSIGNED: The current research work was focused to unveil the in vitro antitumor effects of ononin against the laryngeal cancer Hep-2 cells.
UNASSIGNED: The cytotoxic effects of ononin against the laryngeal cancer Hep-2 cells and normal HuLa-PC laryngeal cells were studied using an 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. The intracellular Reactive Oxygen Species (ROS) generation, apoptotic cell death, Mitochondrial Membrane Potential (MMP), and cell adhesion on the 25 and 50 µM ononin-treated Hep-2 cells were detected using respective staining assays. The levels of TBARS and antioxidants were assayed using specific kits. The expressions of c-Jun N-terminal kinase 1/2 (JNK1/2), Extracellular Signal-regulated Kinase 1/2 (ERK1/2), p38, Phosphatidylinositol-3 Kinase 1/2 (PI3K1/2), and protein kinase-B (Akt) in the ononin-treated Hep-2 cells were investigated using Reverse Transcription-Polymerase Chain Reaction (RT-PCR) assay.
UNASSIGNED: The ononin treatment effectively inhibited the Hep-2 cell viability but did not affect the viability of HuLa-PC cells. Furthermore, the ononin treatment effectively improved the intracellular ROS accumulation, depleted the MMP, and triggered apoptosis in Hep-2 cells. The Thiobarbituric acid reactive substances (TBARS) were improved, and Glutathione (GSH) levels and Superoxide dismutase (SOD) were depleted in the ononin-administered Hep-2 cells. The ononin treatment substantially inhibited the JNK/ERK/p38 axis in the Hep-2 cells.
UNASSIGNED: Together, the outcomes of this exploration proved that the ononin has remarkable antitumor activity against laryngeal cancer Hep-2 cells.