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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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摘要

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/m2). 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)辐射诱导的皮肤损伤,皮肤基质降解,并通过光化学反应和氧化应激皱纹形成。因此,保护​​皮肤免受UVB能防止皮肤老化。在这项研究中,我们调查的混合物皂苷Rg2中,人参皂甙,和虾青素,抗氧化剂的(RA)的影响,在暴露于UVB HaCaT细胞的响应(700焦耳/平方米)。将细胞温育24小时后UVB暴露和细胞存活力通过MTT测定来确定。 UVB相比未处理的对照细胞的60%细胞活力下降,而RA以依赖于浓度的方式增加细胞活力,并且该增加明显低于单一治疗组显著更高。此外,UVB增加的DNA损伤的水平,如环丁烷嘧啶二聚体(CPD)和8-羟基(8-OHdG的)。相反地​​,RA以依赖于浓度的方式既CPD和的8-OHdG水平降低。 UVB暴露也增加突变的共济失调毛细血管扩张症的磷酸化(ATM)蛋白激酶和p53,并随后增加GADD45α,P21,和基质金属蛋白酶(MMPs)的水平-3,-9和-13。另外,UVB暴露COL1A1的水平降低。然而,RA治疗降低对ATM,对P53,GADD45α,P21,MMP-3,水平-9和-13并且以浓度依赖的方式增加COL1A1的水平。这些结果表明,通过RA RG2和虾青素的综合影响通过DNA修复的上调降低UVB诱导的细胞毒性和基因毒性。

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