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咖啡因增强UVB辐射诱导的HaCaT细胞凋亡的研究(1)
http://www.100md.com 2011年7月1日 雷霞 刘渤 何玉英 伍津津 成琼辉
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     [摘要]目的:观察咖啡因对中波紫外线(Ultraviolet B ,UVB)辐射诱导的HaCaT细胞凋亡的影响。方法:在DMEM 中培养HaCaT细胞,将细胞分成空白对照组(A组),1mM咖啡因处理组(B组),5mM咖啡因处理组(C组),UVB(20mJ/cm2)辐射组(D组),UVB辐射(20mJ/cm2)+1mM咖啡因处理组(E组),UVB辐射(20mJ/cm2)+5mM咖啡因处理组(F组),Annexin V/PI观察各组细胞凋亡比例,Western blot检测各组细胞p21和BCL-2表达情况。结果:20mJ/cm2UVB能诱导HaCaT细胞凋亡增加(A组 凋亡率5.43%,D组凋亡率20.67%),而1mM和5mM咖啡因能进一步促进HaCaT细胞凋亡(E组凋亡率22.25%, F组凋亡率36.61%),UVB 抑制细胞p21和BCL-2蛋白表达,咖啡因能进一步抑制21和BCL-2蛋白表达。结论:UVB辐射能诱导HaCaT细胞凋亡,抑制p21和BCL-2蛋白表达,咖啡因则能进一步促进凋亡,抑制p21和BCL-2蛋白表达。

    [关键词]咖啡因;中波紫外线;细胞凋亡

    [中图分类号]Q813.1 [文献标识码]A [文章编号]1008-6455(2011)07-1105-03

    The effect of caffeine to UVB irradiation induced cell apoptosis of HaCaT cells

    LEI Xia1,LIU Bo2,HE Yu-ying3,WU Jin-jin1,CHENG Qiong-hui1

    (1.Department of Dermatology,The Third Affiliated Hospital,The Third Military Medical University,Chongqing 400042,China;2.Department of Orthopaedics,The First Affiliated Hospital,Chongqing Medical University,Chonqing 400036,China;3.Department of Dermatology,University of Chicago,60637,USA)

    Abstract:ObjectiveTo investigate the effect of caffeine on UVB irradiation induced cell apoptosis of HaCaT cells.MethodsHaCaT cells were cultured in DMEM medium. Cells were divided into 6 groups. A group: Blank control (without UVB and caffeine); B group:1mM caffeine, without UVB; C group: 5mM caffeine, without UVB; D group: without caffeine ,20mJ/cm2 UVB; E group: 1mM caffeine, 20mJ/cm2 UVB ; F group: 5mM caffeine, 20mJ/cm2 UVB. Annexin V/PIKit was used to detect cell apoptosis. Western blot was used to detect theexpression of p21 and BCL-2. Results 20mJ/cm2 UVB irradiation could induce cell apoptosis of HaCaT cells (cell apoptosis rate is 5.43% in group A and 20.67% in group D), 1mM and 5mM caffeine could promote cell apoptosis of HaCaT cells further (cell apoptosis rate is 22.25% in group E and 36.61% in group F). UVB irradiation could inhibite the expression of p21 and BCL-2,caffeine could inhibite p21 and BCL-2 futher.ConclusionsUVB irradiation could induce HaCaT cell apoptosis and inhibite the expression ofp21 and BCL-2 ......

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