摘要
【目的】研究咖啡因对UV诱导的HaCaT细胞氧化损伤的影响及其作用机制。【方法】用UV诱导HaCaT构建氧化损伤模型。将HaCaT设置对照组、UV损伤组、不同浓度(50、100μg·mL-1)咖啡因组。结晶紫染色检测细胞生长;特定活性氧指示剂测定胞内及线粒体内活性氧含量;Western blot检测p-p38、p-ERK、p-JNK、MMP9、Acetyl-p53及SIRT3的表达变化。【结果】与对照组相比,UV损伤组细胞存活率显著下降,胞内及线粒体内活性氧含量均显著增加,p-p38、p-JNK、p-ERK、MMP9及Acetyl-p53蛋白表达显著上升而SIRT3蛋白表达显著降低(P<0.05、或P<0.01、或P<0.001)。与UV损伤组相比,不同浓度咖啡因组细胞存活率显著升高,胞内及线粒体内活性氧含量均显著下降,p-p38、p-JNK、p-ERK、MMP9及Acetyl-p53蛋白表达显著降低而SIRT3蛋白表达显著上升(P<0.05、或P<0.01、或P<0.001)。【结论】咖啡因能提高UV氧化损伤后HaCaT的存活率,减少胞内及线粒体内活性氧积累,其通过抑制p-p38、p-JNK、p-ERK、MMP9、Acetyl-p53及促进SIRT3表达而发挥作用。
【Objective】The purpose of this paper is to investigate the effect of caffeine on UV-induced oxidative damage to HaCaT cells and its mechanism.【Method】The oxidative damage model was established by HaCaT cells stimulated by UV irradiation.HaCaT cells were divided into control group,UV damage group,caffeine groups with different concentrations(50,100μg·mL-1).Cell growth was detected by crystal violet staining.Intracellular and mitochondrial reactive oxygen species(ROS)were determined by specific ROS indicators.Expression levels of p-p38,p-ERK,p-JNK,MMP9,Acetyl-p53,and SIRT3 were examined by Western blot.【Result】Compared with the control group,the cell growth of HaCaT was significantly inhibited,the intracellular and mitochondrial ROS and the expression levels of p-p38,p-ERK,p-JNK,MMP9,and Acetyl-p53 were significantly increased,whereas SIRT3 protein significantly decreased,in the UV damage group(P<0.05,or P<0.01,or P<0.001).Compared with the UV damage group,the cell growth of HaCaT was significantly increased,the intracellular and mitochondrial ROS and the expression levels of p-p38,p-ERK,p-JNK,MMP9,and Acetyl-p53 were significantly decreased,whereas SIRT3 protein significantly increased,in the caffeine groups with different concentrations(50,100μg·mL-1)(P<0.05,or P<0.01,or P<0.001).【Conclusion】Caffeine can enhance the survival rate of HaCaT cells after UV induced oxidative damage and reduce the accumulation of intracellular and mitochondrial ROS by inhibiting p-p38,p-ERK,p-JNK,MMP9,Acetyl-p53 and promoting SIRT3.
作者
干春霞
胡财江
王立甜
高梓琪
李今
徐晶
王宣军
盛军
徐欢欢
GAN Chun-xia;HU Ca-jiang;WANG Li-tian;GAO Zi-qi;LI Jin;XU Jing;WANG Xuan-jun;SHENG Jun;XU Huan-huan(Key Laboratory of Pu-er Tea Science,Ministry of Education,Yunnan Agricultural University,Yunnan Kunming 650201,China;College of Food Science and Technology,Yunnan Agricultural Univensity,Yunnan Kunming 650201,China;College of Science,Yunnan Agiculur-al University,Yunnan Kunming 650201,China;State Key Laboratory for Conservation and Utilization of Bio Resources in Yunnan,Yunnan Kunming 650201,China)
出处
《西南农业学报》
CSCD
北大核心
2021年第2期286-292,共7页
Southwest China Journal of Agricultural Sciences
基金
云南省绿色食品国际合作研究中心重点项目(2019ZG00904
2019ZG00909)
云南省科技厅科技计划项目(2018IA060)。
作者简介
干春霞(1995-),女,湖南岳阳人,在读博士研究生,主要从事茶叶功效成分及作用机制研究,E-mail:973920362@qq.com;通讯作者:盛军,E-mail:shengj@ynau.edu.cn;徐欢欢,E-mail:xubuan1017@163.com。
