金枪鱼胶原低聚肽抑制皮肤细胞黑色素生成及抗氧化损伤作用研究

Study on the inhibition of melanogenesis and antioxidant damage of tuna skin collagen oligo-peptide

中文关键词:  金枪鱼胶原低聚肽  黑色素生成  抗氧化  Hacat细胞  氧化损伤

英文关键词:tuna skin collagen oligo-peptide  melanin production  antioxidant  Hacat cells  oxidative damage

中文摘要:

      目的 研究金枪鱼胶原低聚肽(tuna skin collagen oligo-peptide, TSCP)对黑色素生成的抑制作用及其对Hacat细胞氧化损伤的保护效果。方法 通过研究TSCP对B16-f10 细胞黑色素和酪氨酸酶生成的影响, 对B16-f10细胞抗氧化活性分析, 及对双氧水(hydrogen peroxide, H2O2)诱导Hacat细胞氧化损伤的保护作用, 揭示TSCP对黑色素生成的抑制作用及对Hacat细胞氧化损伤的保护机制。结果 TSCP在0.01~1.00 mg/mL质量浓度范围内对B16-f10细胞无明显毒性, 并能显著抑制酪氨酸酶活性和黑色素生成。在1.00 mg/mL质量浓度下, TSCP将黑色素含量降低至83.79%±4.31% (P<0.01), 酪氨酸酶活力降低至78.14%±6.95% (P<0.001)。同时, TSCP显著降低了B16-f10细胞内的活性氧自由基(reactive oxygen species, ROS)水平, 1.00 mg/mL质量浓度下ROS含量下降至53.5%±4.4% (P<0.001), 呈现出良好的抗氧化效果。此外, TSCP能够提升细胞内超氧化物歧化酶(superoxide dismutase, SOD)的活力[(16.62±0.62) U/mg prot, P<0.001], 降低氧化应激标志物丙二醛(malondialdehyde, MDA)的水平[(0.352±0.051) U/mg prot, P<0.001], 并增强谷胱甘肽过氧化物酶(glutathione peroxidase, GSH-Px)的含量[(284.55±4.99) ng/mL, P<0.01]。在Hacat细胞模型中, TSCP同样无显著毒性, 且在H2O2诱导的氧化损伤模型中, TSCP可显著提高细胞存活率, 并抑制细胞凋亡, 1.00 mg/mL TSCP处理后细胞存活率提高至73.66%±5.48% (P<0.01)。结论 TSCP具有显著的抑制黑色素生成和抗氧化活性, 展现出在皮肤美白和抗氧化治疗中的潜在应用价值。

英文摘要:

      Objective To investigate the inhibitory effects of tuna skin collagen oligo-peptide (TSCP) on melanin production and oxidative damage protection in Hacat cells. Methods Through investigated the effects of TSCP on melanin and tyrosinase production in B16-f10 cells, analyzed the antioxidant activity in B16-f10 cells, and assessed its protective effect against hydrogen peroxide (H2O2) induced oxidative damage in Hacat cells, the inhibitory mechanism of TSCP on melanin production and its protective mechanism against oxidative damage in Hacat cells were revealed. Results The experimental results showed that TSCP exhibits no significant cytotoxicity to B16-f10 cells at concentrations ranging from 0.01 to 1.00 mg/mL, and significantly inhibited tyrosinase activity and melanin production. At a concentration of 1.00 mg/mL, TSCP significantly reduced melanin content to 83.79%±4.31% (P<0.01) and tyrosinase activity to 78.14%±6.95% (P<0.001). TSCP also significantly reduced the levels of reactive oxygen species (ROS) in B16-f10 cells. At 1.00 mg/mL, the ROS levels decreased to 53.5%±4.4% of the control group (P<0.001), indicating potent antioxidant potential. Additionally, TSCP increased the activity of superoxide dismutase (SOD) to (16.62±0.62) U/mg prot (P<0.001) and reduced malondialdehyde (MDA) content to (0.352±0.051) U/mg prot (P<0.001). Glutathione peroxidase (GSH-Px) levels were also elevated, reaching (284.55±4.99) ng/mL at 1.0 mg/mL (P<0.01). In the Hacat cell model, TSCP similarly exhibited no significant toxicity and, in the H2O2-induced oxidative damage model, significantly improved cell viability and suppressed apoptosis. At 1.00 mg/mL, TSCP improved cell survival to 73.66%±5.48% (P<0.01), compared to the model group. Conclusion TSCP can inhibit melanin production, reduce oxidative stress, providing a foundation for its potential applications in skin whitening and antioxidant therapies.