文章摘要
唐桦徐晓芃冯浩肖伟荣.白藜芦醇对紫外线照射后人角质形成细胞AQP3 表达的影响[J].,2012,12(12):2275-2277
白藜芦醇对紫外线照射后人角质形成细胞AQP3 表达的影响
Effect of Resveratrol on Expression of Aquaporin 3 in Normal HumanEpidermal Keratinocytes Irradiated by UVB
  
DOI:
中文关键词: 白藜芦醇  水通道蛋白3  角质形成细胞  中波紫外线
英文关键词: Resvetatrol  Aquaporin 3(AQP3)  Normal human epidermal keratinocytes(NHEK)  Ultraviolet B(UVB)
基金项目:
作者单位
唐桦徐晓芃冯浩肖伟荣 湖南省人民医院皮肤科 
摘要点击次数: 874
全文下载次数: 0
中文摘要:
      目的:探讨白藜芦醇对紫外线照射后人皮肤角质形成细胞水通道蛋白3(AQP3)表达的影响及意义。方法:原代培养人皮肤 角质形成细胞,采用UVB(20mJ/cm2,40mJ/cm2)照射角质形成细胞后,立即加入0.1mmol/L 的白藜芦醇进行干预。RT-PCR 检测 照射前后角质形成细胞中AQP3 mRNA 的表达量,并用羟胺法、比色法、TBA 法检测照射前后细胞超氧化物歧化酶(SOD)、谷胱 甘肽过氧化物酶(GSH-Px)活性及丙二醛(MDA)含量。结果:1.UVB 照射后角质形成细胞AQP3 mRNA 的表达量下降(P<0.05), 且UVB 照射剂量越大,AQP3 mRNA 下降越显著(P<0.05)。2.白藜芦醇能显著增加UVB 照射后角质形成细胞SOD 和GSH-Px 活性,并降低细胞MDA 含量(P<0.05)。3.白藜芦醇能显著抑制UVB 导致的角质形成细胞AQP3 mRNA 下降(P<0.05)。结论:白藜 芦醇可能通过抑制UVB 导致的AQP3 mRNA 下降,及提高氧化酶活性、清除自由基的功能,从而延缓皮肤衰老。
英文摘要:
      Objective: To investigate the effect of resveratrol on expression of AQP3 in normal human epidermal keratinocytes (NHEK) irradiated by UVB, and discuss its function in the process of skin aging. Methods: Preparation of skin keratinocyte primary cultures. NHEK irradiated by UVB (20mJ/cm2,40mJ/cm2) were immediately treated with 0.1mmol/L resvetatrol, then observe the change of the expression of AQP3 mRNA by RT-PCR, and the change of SOD, GSH-Px and MDA by Hydroxyl amine method, colorimetric method and TBA method. Results: 1. The expression level of AQP3 mRNA after UVB irradiation was significantly lower than its level before UVB irradiation (P<0.05). The more the UVB exposure dose it received, the greater the expression level of AQP3 mRNA decreased. 2. Resvetatrol increased the activity of SOD and GSH-Px, decreased MDA's content of NHEK irradiated by UVB (P<0.05). 3. Resvetatrol inhibited the decrease of AQP3 mRNA irradiated by UVB (P<0.05). Conclusion: Resvetatrol can attenuate UVB-induced down-regulation of AQP3, increase oxydase's activity and clean the free radical, and accordingly to delay skin aging.
查看全文   查看/发表评论  下载PDF阅读器
关闭