首页> 外文期刊>Journal of cellular biochemistry. >Curcumin inhibits UV irradiation-induced oxidative stress and apoptotic biochemical changes in human epidermoid carcinoma A431 cells.
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Curcumin inhibits UV irradiation-induced oxidative stress and apoptotic biochemical changes in human epidermoid carcinoma A431 cells.

机译:姜黄素抑制人表皮样癌A431细胞中紫外线辐射诱导的氧化应激和凋亡生化变化。

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Ultraviolet (UV) light is a strong apoptotic trigger that induces caspase-dependent biochemical changes in cells. Previously we showed that UV irradiation can activate caspase-3, and the subsequent cleavage and activation of p21(Cdc42/Rac)-activated kinase 2 (PAK2) in human epidermoid carcinoma A431 cells. In this study we demonstrate that curcumin (Cur), the yellow pigment of Curcuma longa with known anti-oxidant and anti-inflammatory properties, can prevent UV irradiation-induced apoptotic changes, including c-Jun N-terminal kinase (JNK) activation, loss of mitochondrial membrane potential (MMP), mitochondrial release of cytochrome C, caspase-3 activation, and cleavage/activation of PAK2 in A431 cells. Flow cytometric analysis using the cell permeable dye 2',7'-dichlorofluorescin diacetate (DCF-DA) as an indicator of reactive oxygen species (ROS) generation revealed that the increase in intracellular oxidative stress caused by UV irradiation could be abolished by Cur. In addition, we found that SP600125, a JNK-specific inhibitor, reduced UV irradiation-induced JNK activation as well as caspase-3 activation, indicating that JNK activity is required for UV irradiation-induced caspase activation. Collectively, our results demonstrate that Cur significantly attenuates UV irradiation-induced ROS formation, and suggest that ROS triggers JNK activation, which in turn causes MMP change, cytochrome C release, caspase activation, and subsequent apoptotic biochemical changes. J. Cell. Biochem. 90: 327-338, 2003.
机译:紫外线(UV)是强烈的凋亡触发因子,可诱导细胞中caspase依赖性生化变化。先前我们表明,紫外线照射可以激活人表皮样癌A431细胞中的caspase-3,以及随后对p21​​(Cdc42 / Rac)激活的激酶2(PAK2)的裂解和激活。在这项研究中,我们证明姜黄素(Cur)是姜黄的黄色素,具有已知的抗氧化和抗炎特性,可以阻止UV辐射诱导的细胞凋亡变化,包括c-Jun N端激酶(JNK)活化,线粒体膜电位(MMP)的丧失,线粒体细胞色素C的释放,caspase-3激活以及PA431在PA431中的裂解/激活。使用细胞可渗透染料2',7'-二氯荧光素二乙酸盐(DCF-DA)作为活性氧(ROS)生成指示剂的流式细胞仪分析表明,Cur可以消除由UV辐射引起的细胞内氧化应激的增加。此外,我们发现JNK特异性抑制剂SP600125减少了UV辐射诱导的JNK活化以及caspase-3活化,表明JNK活性是UV辐射诱导的caspase活化所必需的。总体而言,我们的结果表明,Cur可显着减弱UV辐射诱导的ROS形成,并暗示ROS触发JNK激活,进而引起MMP变化,细胞色素C释放,胱天蛋白酶激活以及随后的凋亡生化变化。 J.细胞。生化。 90:327-338,2003。

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