文献类型：期刊文献

中文题名：黄芪多糖对中波紫外线辐射皮肤角质形成细胞损伤的影响

英文题名：Effects of Astragalus Polysaccharides on Damage of Keratinocytes in UVB Radiation Skin

作者：李杨[1];安方玉[1];明海霞[1];刘永琦[1]

第一作者：李杨

机构：[1]甘肃中医药大学甘肃省高校重大疾病分子医学与中医药防治研究重点实验室,甘肃兰州730000

第一机构：甘肃中医药大学科研实验中心（甘肃省中医药标准化技术委员会秘书处）

年份：2016

卷号：23

期号：5

起止页码：44

中文期刊名：中国中医药信息杂志

外文期刊名：Chinese Journal of Information on Traditional Chinese Medicine

收录：CSTPCD;;CSCD:【CSCD_E2015_2016】；

基金：甘肃省高校重大疾病分子医学与中医药防治研究省级重点实验室培育基金项目(2013年)

语种：中文

中文关键词：黄芪多糖;中波紫外线;皮肤角质形成细胞;保护作用

外文关键词：Astragalus polysaccharides;;ultraviolet B;;Ha Ca T cells;;protective effect

摘要：目的观察黄芪多糖对中波紫外线(UVB)辐射损伤皮肤角质形成细胞(Ha Ca T细胞)的影响,初步探讨其作用机制。方法采用UVB辐射Ha Ca T细胞进行造模。分为空白对照组、模型组、阳性对照组及黄芪多糖低、中、高剂量组,各药物组给予相应药物干预。MTT法测定细胞活力;生化比色法检测谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、丙二醛(MDA)含量;ELISA检测肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)含量。结果与空白对照组比较,模型组SOD、CAT、GSH-Px含量降低,MDA、TNF-α、IL-6含量升高(P<0.05);与模型组比较,各药物组SOD、GSH-Px、CAT含量升高,MDA、TNF-α、IL-6含量降低(P<0.01)。结论黄芪多糖可在一定程度上减轻UVB对Ha Ca T细胞氧化应激性损伤。
Objective To investigate the effects of Astragalus polysaccharide (APS) on damage of keratinocytes in ultraviolet B (UVB) radiation skin in HaCaT cells; To preliminarily explore its mechanism of action.Methods HaCaT cells were treated by UVB irradiated for modeling. Blank control group, model group, UVB irradiation group and low-, medium- and high-dose APS interventional groups were set up. Each medication group was given relevant medicine. MTT assay was used to determine the cell activity; GSH-Px, CAT, SOD activity and MDA content were detected by biochemical colorimetric method; contents of TNF-α and IL-6 were detected by ELISA.Results Compared with the control group, the contents of SOD, CAT and GSH-Px in the model group decreased significantly, while the contents of MDA, TNF-α and IL-6 increased significantly (P<0.05); compared with the mode group, the contents of SOD, CAT and GSH-Px in the medication groups increased significantly, while the contents of MDA, TNF-α and IL-6 were reduced significantly (P<0.01).Conclusion APS can reduce the oxidative stress injury of UVB to HaCaT cells to some extent.