首页> 外文期刊>Archives of Toxicology >Apoptosis initiation of β-ionone in SGC-7901 gastric carcinoma cancer cells via a PI3K-AKT pathway.
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Apoptosis initiation of β-ionone in SGC-7901 gastric carcinoma cancer cells via a PI3K-AKT pathway.

机译:通过PI3K-AKT途径在SGC-7901胃癌细胞中β电离机的凋亡引发。

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摘要

β-ionone has been shown to hold potent anti-proliferative and apoptosis induction properties in vitro and in vivo. To investigate the effects of β-ionone on apoptosis initiation and its possible mechanisms of action, we qualified cell apoptosis, proteins related to apoptosis and a phosphatidylinositol 3-kinase (PI3K)-AKT pathway in human gastric adenocarcinoma cancer SGC-7901 cells. The results demonstrated that β-ionone-induced apoptosis in a dose-dependent manner in SGC-7901 cells treated with β-ionone (25, 50, 100 and 200?μmol/L) for 24?h. β-ionone was also shown to induce the expression of cleaved-caspase-3 and inhibit bcl-2 expression in SGC-7901 cells in a dose-dependent manner. The significantly decreased levels of p-PI3K and p-AKT expression were observed in SGC-7901 cells after β-ionone treatments in a time- and dose-dependent manner (P?
机译:已显示β-离子团在体外和体内保持有效的抗增殖性和凋亡诱导性质。为了探讨β-离子酮对凋亡引发的影响及其可能的作用机制,我们合格细胞凋亡,与凋亡相关的蛋白质和人胃腺癌癌症SGC-7901细胞中的磷脂酰肌醇3-激酶(PI3K)-AKT途径。结果表明,在用β-离子(25,50,100和200μmol/ L)处理的SGC-7901细胞中,β-离子团诱导的凋亡以剂量依赖性方式(25,50,100和200μmol/ L)。还显示β-离子团以诱导裂解 - caspase-3的表达,以剂量依赖性方式抑制在SGC-7901细胞中的Bcl-2表达。在β-离子在β-离子处理后的时间和剂量依赖性方式(p≤0.01),在SGC-7901细胞中观察到P-PI3K和P-AKT表达的显着降低。因此,可以通过PI3K-AKT途径调节SGC-7901细胞中的凋亡诱导。这些结果证明了β-离子诱导SGC-7901细胞中凋亡引发的潜在机制。

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