首页> 美国卫生研究院文献>Molecules >Protective Effects of Chlorella-Derived Peptide Against UVC-Induced Cytotoxicity through Inhibition of Caspase-3 Activity and Reduction of the Expression of Phosphorylated FADD and Cleaved PARP-1 in Skin Fibroblasts
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Protective Effects of Chlorella-Derived Peptide Against UVC-Induced Cytotoxicity through Inhibition of Caspase-3 Activity and Reduction of the Expression of Phosphorylated FADD and Cleaved PARP-1 in Skin Fibroblasts

机译:小球藻衍生肽通过抑制Caspase-3活性和减少磷酸化FADD和切割的PARP-1在皮肤成纤维细胞中的表达而对UVC诱导的细胞毒性的保护作用。

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摘要

UVC irradiation induces oxidative stress and leads to cell death through an apoptotic pathway. This apoptosis is caused by activation of caspase-3 and formation of poly(ADP-ribose) polymerase-1 (PARP-1). In this study, the underlying mechanisms of Chlorella derived peptide (CDP) activity against UVC-induced cytotoxicity were investigated. Human skin fibroblasts were treated with CDP, vitamin C, or vitamin E after UVC irradiation for a total energy of 15 J/cm2. After the UVC exposure, cell proliferation and caspase-3 activity were measured at 12, 24, 48, and 72 h later. Expression of phosphorylated FADD and cleaved PARP-1 were measured 16 h later. DNA damage (expressed as pyrimidine (6-4) pyrimidone photoproducts DNA concentration) and fragmentation assay were performed 24 h after the UVC exposure. Results showed that UVC irradiation induced cytotoxicity in all groups except those treated with CDP. The caspase-3 activity in CDP-treated cells was inhibited from 12 h onward. Expression of phosphorylated FADD and cleaved PARP-1 were also reduced in CDP-treated cells. Moreover, UVC-induced DNA damage and fragmentation were also prevented by the CDP treatment. This study shows that treatment of CDP provides protective effects against UVC-induced cytotoxicity through the inhibition of caspase-3 activity and the reduction of phosphorylated FADD and cleaved PARP-1 expression.
机译:UVC辐射诱导氧化应激并通过凋亡途径导致细胞死亡。这种凋亡是由caspase-3的激活和聚(ADP-核糖)聚合酶1(PARP-1)的形成引起的。在这项研究中,研究了小球藻衍生肽(CDP)活性对UVC诱导的细胞毒性的潜在机制。 UVC照射后,人类皮肤成纤维细胞用CDP,维生素C或维生素E处理,总能量为15 J / cm 2 。在暴露于UVC之后,在12、24、48和72小时后测量细胞增殖和caspase-3活性。 16小时后测量磷酸化的FADD和裂解的PARP-1的表达。在UVC暴露24小时后进行DNA损伤(表示为嘧啶(6-4)嘧啶酮光产物DNA浓度)和片段化测定。结果表明,除了用CDP处理的那些外,UVC辐射在所有组中均引起细胞毒性。从12小时起,CDP处理的细胞中的caspase-3活性被抑制。在CDP处理的细胞中,磷酸化的FADD和裂解的PARP-1的表达也降低了。此外,CDP处理还可以防止UVC诱导的DNA损伤和片段化。这项研究表明CDP的治疗可通过抑制caspase-3活性,减少磷酸化的FADD和裂解的PARP-1表达来提供抗UVC诱导的细胞毒性的保护作用。

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