目的 探讨白及多糖对氯化钴( CoCl2)诱导人角质形成细胞(HKC)氧化应激形成炎症损伤的JAK/STAT信号通路的保护作用机制.方法 用白及多糖对HKC进行预处理后,用CoCl2处理HKC细胞,建立化学性低氧化剂诱导皮肤细胞氧化应激导致炎症损伤的细胞模型,以噻唑蓝法检测细胞生存活率,用酶联免疫吸附( ELISA)法检测细胞培养液中白细胞介素(IL)-6和IL-8的水平；以ELISA法检测细胞上清液中肿瘤坏死因子(TNF)-α的分泌量,检测JAK2蛋白的表达.结果 白及多糖提高CoCl2诱导角质形成细胞的存活率具有剂量依赖性.白及多糖高、中剂量组TNF-α、IL-6和IL-8含量与CoCl2对照组比较差异有统计学意义(P＜0.05).结论 CoCl2通过产生氧化应激反应导致HKC炎症损伤；白及多糖通过调节JAK/STAT信号通路的JAK2表达水平抑制TNF-α、IL-6和IL-8的释放,可能是其对HKC抗氧化损伤保护作用机制之一.%Objective To investigate the protective effect and mechanism of Bletilla Striata polysaccharide on JAK/ STAT signaling pathway in human keratinocytes (HKCs) with inflammation induced injury by CoCl2. Methods After pretreated with Bletilla Striatu polysaccharide, HKCs were interfered with certain dosages of CoCl2 to establish an inflammation induced injury cell model by oxidative stress from chemical oxidizing agent. The cell viability was detected by MTT method. The levels of cytokine TNF-α, IL-6 and IL-8 were detected by ELISA, and expression of JAK2 was determined. Results Bletilla Striata polysaccharide could boost the cell viability in a dose-dependent manner. The contents of TNF-α, IL-6 and IL-8 in the group of high or medium dosage of Bletilla Striata polysaccharide were significantly different from those in the control group (P< 0.05). Conclusion The inflammation injury of HKC can be caused by oxidative stress from CoCl2. Btetilla Striata polysaccharide can inhibit release of TNF-α, IL-6 and IL-8 through regulating expression of JAK2 in JAK/STAT signaling pathway, which might be one of the mechanisms of protection.
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