Faculty of Pharmaceutical Sciences, Tokyo University of Science, Noda-shi, Chiba, Japan.
J Toxicol Sci. 2011;36(6):741-50. doi: 10.2131/jts.36.741.
It has recently been reported that activation of P2Y(1) receptor, one of the purine receptors, by extracellular nucleotides induces cytoprotection against oxidative stress. In this study, we examined the protective effect of ATP on the cell damage in human epidermal keratinocyte HaCaT cells exposed to H(2)O(2) via the P2Y receptor-mediated induction of intracellular antioxidants. The cells were damaged by exposure to H(2)O(2) in a dose- and time-dependent manner. The damage induced by 7.5 mM H(2)O(2) was blocked by pretreatment of the cells with ATP (1-10 µM). The protective effect of ATP was significantly reduced by P2Y receptor antagonists. Exogenously added ATP induced various intracellular antioxidants, including thiol-containing proteins, Cu/Zn superoxide dismutase (SOD) and thioredoxin-1, in HaCaT cells. In conclusion, it was found that ATP protected the cells from the H(2)O(2)-induced cell damages via the P2Y receptor-mediated induction of intracellular antioxidants.
最近有报道称，细胞外核苷酸激活嘌呤受体之一 P2Y(1)受体可诱导细胞对抗氧化应激产生保护作用。在这项研究中，我们通过 P2Y 受体介导的细胞内抗氧化剂的诱导，研究了 ATP 对暴露于 H2O2 的人表皮角质形成细胞 HaCaT 细胞的细胞损伤的保护作用。细胞以剂量和时间依赖的方式暴露于 H2O2 中受到损伤。用 1-10 µM ATP 预处理细胞可阻断 7.5 mM H2O2 诱导的损伤。P2Y 受体拮抗剂显著降低了 ATP 的保护作用。外源性添加的 ATP 诱导了 HaCaT 细胞中的各种细胞内抗氧化剂，包括含巯基蛋白、Cu/Zn 超氧化物歧化酶（SOD）和硫氧还蛋白-1。总之，研究发现 ATP 通过 P2Y 受体介导的细胞内抗氧化剂的诱导，保护细胞免受 H2O2 诱导的细胞损伤。
