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Protective effects of ginsenoside Rg2 and astaxanthin mixture against UVB-induced DNA damage

机译:人参皂苷Rg2和虾青素混合物对UVB诱导的DNA损伤的保护作用

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Ultraviolet B (UVB) radiation induces skin damage, skin matrix degradation, and wrinkle formation through photochemical reaction and oxidative stress. Therefore, protecting the skin from UVB can prevent skin aging. In this study, we investigated the effects of a mixture (RA) of Rg2, a ginsenoside, and astaxanthin, an antioxidant, on the responses of HaCaT cells exposed to UVB (700?J/m~(2)). The cells were incubated for 24?h after UVB exposure and cell viability was determined by MTT assay. UVB decreased cell viability by 60% compared to that of untreated control cells, whereas RA increased cell viability in a concentration-dependent manner, and this increase was significantly higher than that in the single treatment groups. Further, UVB increased the levels of DNA lesions such as cyclobutane pyrimidine dimer (CPD) and 8-hydroxyguanine (8-OHdG). Conversely, RA decreased both CPD and 8-OHdG levels in a concentration-dependent manner. UVB exposure also increased phosphorylation of ataxia-telangiectasia mutated (ATM) protein kinase and p53 and subsequently increased the levels of GADD45α, p21, and matrix metalloproteinases (MMPs)-3, -9, and -13. Additionally, UVB exposure decreased the level of COL1A1. However, RA treatment decreased the levels of p-ATM, p-p53, GADD45α, p21, MMP-3, -9, and -13 and increased the level of COL1A1 in a concentration-dependent manner. These results suggest that RA reduces UVB-induced cytotoxicity and genotoxicity through up-regulation of DNA repair via the combined effects of Rg2 and astaxanthin.
机译:紫外线B(UVB)辐射通过光化学反应和氧化应激引起皮肤损伤,皮肤基质降解和皱纹形成。因此,保护​​皮肤免受UVB污染可以防止皮肤老化。在这项研究中,我们研究了人参皂苷Rg2和抗氧化剂虾青素的混合物(RA)对暴露于UVB(700?J / m〜(2))的HaCaT细胞反应的影响。 UVB暴露后将细胞孵育24小时,并通过MTT测定法测定细胞活力。与未处理的对照细胞相比,UVB将细胞活力降低了60%,而RA以浓度依赖的方式提高了细胞活力,并且这种增加明显高于单个处理组。此外,UVB增加了DNA损伤的水平,例如环丁烷嘧啶二聚体(CPD)和8-羟基鸟嘌呤(8-OHdG)。相反,RA以浓度依赖性方式降低了CPD和8-OHdG的水平。 UVB暴露还增加了共济失调-毛细血管扩张突变(ATM)蛋白激酶和p53的磷酸化,随后增加了GADD45α,p21和基质金属蛋白酶(MMPs)-3,-9和-13的水平。此外,UVB暴露会降低COL1A1的水平。但是,RA治疗降低了p-ATM,p-p53,GADD45α,p21,MMP-3,-9和-13的水平,并以浓度依赖的方式增加了COL1A1的水平。这些结果表明,RA通过Rg2和虾青素的联合作用,通过上调DNA修复来降低UVB诱导的细胞毒性和基因毒性。

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