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作 者:陈巧云[1] 杨柳 刘斌[1] 李文鹏 李伟[1] 谷建梅[1] 黄昕红[1] 尤棵 王业秋[1] CHEN Qiaoyun;YANG Liu;LIU Bin;LI Wenpeng;LI Wei;GU Jianmei;HUANG Xinhong;YOU Ke;WANG Yeqiu(Jiamusi College of Heilongjiang University of Chinese Medicine,Jiamusi 154007,China)
机构地区:[1]黑龙江中医药大学佳木斯学院,黑龙江佳木斯154007
出 处:《中医药信息》2021年第6期41-44,共4页Information on Traditional Chinese Medicine
基 金:黑龙江卫生计生委科研课题(2017-578);黑龙江中医药管理局科研项目(ZHY16-102);黑龙江省大学生创新创业训练计划项目(201910228046)。
摘 要:目的:探讨京尼平苷对UVA诱导HSF细胞凋亡相关蛋白p53、Bax、Bcl-2 mRNA表达的影响。方法:用20 J/cm的UVA照射HSF细胞,建立光损伤模型,以5×10^(-7)、5×10^(-6)、5×10^(-5) mol/L京尼平苷干预光损伤细胞,检测细胞活力、ROS相对含量、LDH活性,细胞凋亡率,实时定量PCR法检测p53、Bax、Bcl-2 mRNA的表达。结果:与空白对照组相比,UVA照射后,ROS相对含量增加,LDH活性增强,细胞活力下降,p53、Bax mRNA表达量升高(P<0.01),Bcl-2 mRNA表达量的降低程度没有统计学意义(P>0.05);在给予京尼平苷干预后,ROS相对含量减少,LDH活性降低,细胞活力增加,p53、Bax mRNA表达量降低,Bcl-2 mRNA及表达量升高(均P<0.05)。结论:京尼平苷通过调控光损伤HSF细胞活力和细胞内ROS含量、LDH活性,调控p53、Bax和Bcl-2 mRNA表达,抑制凋亡相关通路,拮抗细胞的氧化损伤,减少细胞凋亡,起到防治紫外线对皮肤细胞损伤的作用。Objective:To study the effects of geniposide on the mRNA expressions of apoptosis related proteins of p53,Bax and Bcl-2 in HSF cells induced by UVA.Methods:The light damage model of HSF cells was established by irradiation of 20 J/cm UVA.The damaged cells were intervened with different concentrations of geniposide(5×10^(-7),5×10^(-6),5×10^(-5) mol/L).Cell viability,relative content of ROS,LDH activity and apoptosis rate were measured.The mRNA expressions of p53,Bax and Bcl-2 were detected by real-time quantitative PCR.Results:After 20 J/cm UVA irradiation,ROS relative content increased,LDH activity enhanced,cell viability decreased,and the mRNA expressions of Bax and p53 increased(P<0.01),however the decrease of Bcl-2 mRNA expression was not significant when compared to the blank group(P>0.05).After geniposide intervention,ROS relative content reduced,LDH activity decreased,cell viability increased,and the mRNA expressions of Bax and p53 decreased(P<0.05),Bcl-2 mRNA expression increased(P<0.05).Conclusion:Geniposide can inhibit relative pathways,antagonize the oxidative damage of cells,reduce cell apoptosis and prevent skin light damage by improving the activity of ROS and LDH,as well as by regulating the mRNA expressions of p53,Bax and Bcl-2.
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