首页> 外文期刊>Regulatory peptides. >Polypeptide from Chlamys farreri modulates UVB-induced activation of NF-kappaB signaling pathway and protection HaCaT cells from apoptosis.
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Polypeptide from Chlamys farreri modulates UVB-induced activation of NF-kappaB signaling pathway and protection HaCaT cells from apoptosis.

机译:来自衣原体的多肽可调节UVB诱导的NF-κB信号通路的激活,并保护HaCaT细胞免于凋亡。

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摘要

Polypeptide from Chlamys farreri (PCF) possesses strong antioxidant and photochemo-preventive properties. Our previous study has preliminarily demonstrated that PCF could reduce the intracellular reactive oxygen species (ROS) production and protect UVB-induced HaCaT cells apoptosis. But the anti-apoptotic effects of PCF on components of cell signaling pathways leading to gene expression has not been clearly established. In this study we determined whether PCF affords protection of HaCaT cells against UVB-mediated activation of nuclear factor kappa B signal pathway, which is involved in apoptosis. The result showed that pretreatment of UVB-induced HaCaT cells with PCF, ROS scavenger NAC and NF-kappaB inhibitor MG132 effectively suppressed the apoptosis of HaCaT cells. PCF inhibited UVB-induced activation and translocation of NF-kappaB/p65 to nucleus, which was mediated through inhibition of phosphorylation/degradation and decreasing mRNA expression of IkappaBalpha and also blocking activation of IKKalpha in a dose-dependent manner. Furthermore, we observed that NAC also inhibited UVB-induced activation of NF-kappaB/p65 through decreasing the degradation and phosphorylation of IkappaBalpha. We concluded that the activation of NF-kappaB signal pathway played an important role in UVB-induced apoptosis, and PCF likely exerted its anti-apoptotic effect in HaCaT cells through decreasing intracellular ROS level and modulating the NF-kappaB signaling pathway.
机译:衣原体衣原体(PCF)的多肽具有很强的抗氧化剂和光化学防护性能。我们先前的研究已初步证明PCF可以减少细胞内活性氧(ROS)的产生并保护UVB诱导的HaCaT细胞凋亡。但是,尚未明确建立PCF对导致基因表达的细胞信号通路成分的抗凋亡作用。在这项研究中,我们确定PCF是否提供针对HaCaT细胞的保护,使其免受UVB介导的参与凋亡的核因子kappa B信号通路的激活。结果表明,用PCF,ROS清除剂NAC和NF-κB抑制剂MG132预处理UVB诱导的HaCaT细胞可有效抑制HaCaT细胞凋亡。 PCF抑制UVB诱导的NF-κB/ p65活化和易位至细胞核,这是通过抑制IkappaBalpha的磷酸化/降解和降低mRNA表达来介导的,并且还以剂量依赖的方式阻断IKKalpha的活化。此外,我们观察到NAC还通过减少IkappaBalpha的降解和磷酸化来抑制UVB诱导的NF-kappaB / p65的活化。我们得出的结论是,NF-κB信号通路的激活在UVB诱导的细胞凋亡中起重要作用,而PCF可能通过降低细胞内ROS水平并调节NF-κB信号通路而在HaCaT细胞中发挥其抗凋亡作用。

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