项目名称: 秦苓液调控AMPK信号系统抑制尿酸性肾病免疫代谢炎性损伤的分子机制研究
项目编号: No.81473516
项目类型: 面上项目
立项/批准年度: 2015
项目学科: 医药、卫生
项目作者: 孟凤仙
作者单位: 北京中医药大学
项目金额: 72万元
中文摘要: 尿酸性肾病的发病机制与多因素相关。尿酸作为前炎性因子介导的免疫代谢炎性网络通路是尿酸性肾损害机制的核心环节。我们在完成国家自然基金课题的后续研究中发现,秦苓液显著上调尿酸性肾病大鼠肾组织腺苷酸活化蛋白激酶(AMPK)基因转录及蛋白表达水平。由此推论:该方抑制尿酸性肾损害的分子机制可能由其诱导激活免疫代谢炎性抑制因子AMPK上游信号系统完成。故本项目在原工作基础上,从秦苓液对AMPK信号通路的调控机制及其对介导尿酸性肾损害的关键免疫炎性分子的干预途径、作用机制研究入手,在基因和蛋白质水平,采用体内外试验相结合的方式,研究秦苓液对AMPK磷酸化活性的影响,研究秦苓液作用下通过siRNA调控AMPK表达水平对下游分子信号通路的影响机制。探讨秦苓液抑制尿酸性肾病免疫代谢炎性损伤的作用靶点及上游环节。为丰富本病治疗寻找新突破,为AMPK在免疫代谢炎性疾病领域中的生物学效应研究奠定基础。
中文关键词: 秦苓液;AMPK信号系统;尿酸性肾病;分子机制
英文摘要: Hyperuricemic nephropathy is related with many factors. The network immunological metabolic inflammatory pathways mediated by uric acid, a pro-inflammatory cytokine, is the core factor for renal damage.We found, in the subsequent research supported by the National Natural Science Foundation of China, that Qinlingye significantly up-regulated the gene and protein expression of the nephridial tissue's adenosine monophosphate-activated protein kinase (AMPK) in rats with Hyperuricemic nephropathyInference: Qinlingye may induce and activate the up-stream signals of the immunological metabolic inflammation inhibitory cytokine AMPK to repress hyperuricemic renal impairment.On the basis of our finished work, in this study, we will, focusing on how Qinlingye regulates AMPK signaling pathway and effects the key immunological metabolic cytokines mediating renal impairment, research in Qinlingye's effect on AMPK phosphorylation activity and siRNA regulation on AMPK and its downstream signaling pathways, thus to explore the target of Qinlingye represses immunological metabolic inflammatory impairment of hyperuricemic nephropathy.
英文关键词: qinglingye(QLY);AMPK signaling pathway;uric acid renal damage;molecular mechanism