中文摘要：

目的探讨桃叶珊瑚苷对紫外线B波损伤的皮肤角质形成细胞的保护作用及其机制。方法用64mJ·cm-2的紫外线B波照射角质形成细胞建立光损伤模型，以不同浓度桃叶珊瑚苷处理损伤细胞，四甲基偶氮唑蓝法检测细胞活力，用试剂盒分别检测细胞中超氧化物歧化酶活性、谷胱甘肽过氧化酶活性、过氧化氢酶活性、丙二醛含量，逆转录-聚合酶链反应法检测细胞中P38、肿瘤坏死因子-α．及白介素-6mRNA的表达量，酶联免疫法检测细胞上清液中肿瘤坏死因子-α．及白介素-6的含量。结果紫外线B波照射细胞后，细胞活力、超氧化物歧化酶活性、谷胱甘肽过氧化酶活性、过氧化氢酶活性明显降低，丙二醛含量、P38mRNA表达量、肿瘤坏死因子-α和白介素-6mRNA及蛋白的表达量明显升高（P〈0．01）；1×10^-5和1×10^-6mol·L-1桃叶珊瑚苷能够显著改善角质形成细胞的光损伤（P〈0．05或P〈0．01）。结论桃叶珊瑚苷能改善紫外线B波对角质形成细胞的光损伤，其机制可能与抑制氧化损伤，调控P38信号通路，调节肿瘤坏死因子-α和白介素-6的表达有关。

英文摘要：

OBJECTIVE To investigate the protection of aucubin on keratinocyte damaged by Ultraviolet B and explore its possi- ble mechanism. METHODS The photo damage model of keratinocyte was established by irradiating of UVB （64 mJ. cm-2）. The different concentration aucubin were used for damaged cell. The cell viability was detected by MTT, the SOD activity, GSH-Px activi- ty, CAT activity, MDA content were assayed by kit respectively. The mRNA levels of P38, TNF-α and IL-6 were determined by RT- PCR. The secretion levels of TNF-α and IL-6 of cultured keratinocyte were detected by ELISA. RESULTS After the UVB irradiation, the cell viability, the activities of SOD, GSH-Px and CAT were decreased, the content of MDA,TNF-α and IL-6, the mRNA levels of P38, TNF-α and IL-6 were increased（ P 〈 0.01 ）. The above changes were inhibited by 1 × 10 -5 and 1 × 10 -6 mol. L-1 aucubin （ P 〈 0. 05 or P 〈 0. 01 ）. CONCLUSION The aueubin could inhibit the injury by UVB for keratinocyte. And its possible mechanism may have relationship with the inhibition of oxidative damage, regulatory P38 signal pathway, adjusting the expression of TNF-α and IL-6.