目的探讨血浆致动脉硬化指数(atherogenic index of plasma,AIP)与冠状动脉Gensini评分的相关性。方法选取经冠状动脉造影检查确诊的冠心病患者301例,根据冠状动脉造影结果进行Gensini评分评价冠脉病变程度。结果 AIP值在冠状动脉Gensin...目的探讨血浆致动脉硬化指数(atherogenic index of plasma,AIP)与冠状动脉Gensini评分的相关性。方法选取经冠状动脉造影检查确诊的冠心病患者301例,根据冠状动脉造影结果进行Gensini评分评价冠脉病变程度。结果 AIP值在冠状动脉Gensini评分各亚组的比较差异均具有统计学意义(P <0. 05),并随Gensini评分的升高而逐渐升高。对可能影响冠状动脉Gensini评分的变量做Logstic回归分析,结果显示血浆LDL-C、AIP值是冠状动脉狭窄病变的独立危险因素,HDL-C是独立保护因素。AIP与Gensini评分线性相关分析显示AIP与Gensini评分呈正相关(r=0. 303,P <0. 01)。结论 AIP与冠状动脉Gensini评分密切相关,AIP水平愈高,冠状动脉狭窄愈严重。展开更多
OBJECTIVE To investigate the protective effect of icariin(ICA) on lipopolysaccharide(LPS)-induced BV2 microglia injury,and to clarify the role of nuclear factor erythroid 2-related factor 2(Nrf2) signaling pathway in ...OBJECTIVE To investigate the protective effect of icariin(ICA) on lipopolysaccharide(LPS)-induced BV2 microglia injury,and to clarify the role of nuclear factor erythroid 2-related factor 2(Nrf2) signaling pathway in BV2 microglia-mediated neuroinflammation.METHODS BV2 microglia were randomly divided into control,ICA(0.1 μmol·L^(-1)),LPS(1 mg·L^(-1)),LPS + ICA(0.01 μmol·L^(-1)),and LPS + ICA(0.1 μmol·L^(-1))groups.BV2 microglia were treated with ICA for 30 min and then treated with LPS for 24 h.MTT assay was used to determine the cells survival rate,Griess kit and ELISA kits were used to detect the contents of NO,IL-1β and IL-18 in the culture supernatant,Western blotting was used to detect the expression of Nrf2,HO-1 and NQO1.Real time RT-PCR was used to detect the expression of Nrf2,HO-1 and NQO1 after ICA addition for 2,6 and 24 h.And immunofluorescence was used to observe the activation of Nrf2.RESULTS ICA reduced LPS-induced NO,IL-1β and IL-18 production in the culture supernatant,and ICA increase LPS-induced mRNA and protein expression of Nrf2 signaling pathway.CONCLUSION ICA protects LPS induced neuroinflammation by regulating Nrf2 signaling pathway.展开更多
OBJECTIVE Astroglia support neurons by providing substrates for neuronal metabolism, glutamate clearance and anti-oxidant protection. Nuclear factor erythroid 2-related factor 2(Nrf2) is the main switch of intracellul...OBJECTIVE Astroglia support neurons by providing substrates for neuronal metabolism, glutamate clearance and anti-oxidant protection. Nuclear factor erythroid 2-related factor 2(Nrf2) is the main switch of intracellular antioxidant defense system. Also, Nrf2 signaling is recognized to activate the neurotrophic pathway to replace/protect damaged organelles. Ellagic acid(EA), an excretion component of fruits and nuts, displays anti-oxidant, cardioprotective and antiinflammatory activities. However, few studies have been focused on the neurotrophic properties of EA. Our study investigated whether EA could enhance astroglia neurotrophic effects to support neurons and the underlying mechanisms as well. METHODS Primary neuron-enriched cultures, primary astroglia-enriched cultures and primary neuron-astroglia co-cultures were applied to detect whether pharmacological regulation of astroglia function by EA could be utilized to overcome neuronal death. RESULTS This study indicated that EA promoted neuronal survival. Furtherly, astroglia Nrf2 participate in EA-elicited neuronal survival with the following scenarios. First, EA induced astroglia proliferation, neurotrophic factors release and Nrf2 activation. Second, astroglia-targeted Nrf2 si RNA inhibited EA-mediated astrogliosis,neurotrophic factors excretion and neuronal survival. CONCLUSION EA mediated astroglia Nrf2 activation to enhanced neurotrophic effects on neurons, and these findings might provide new strategies for neurotrophic factor-based treatment of neurodegenerative disease.展开更多
基金National Natural Science Foundation of China(81760658).
文摘OBJECTIVE To investigate the protective effect of icariin(ICA) on lipopolysaccharide(LPS)-induced BV2 microglia injury,and to clarify the role of nuclear factor erythroid 2-related factor 2(Nrf2) signaling pathway in BV2 microglia-mediated neuroinflammation.METHODS BV2 microglia were randomly divided into control,ICA(0.1 μmol·L^(-1)),LPS(1 mg·L^(-1)),LPS + ICA(0.01 μmol·L^(-1)),and LPS + ICA(0.1 μmol·L^(-1))groups.BV2 microglia were treated with ICA for 30 min and then treated with LPS for 24 h.MTT assay was used to determine the cells survival rate,Griess kit and ELISA kits were used to detect the contents of NO,IL-1β and IL-18 in the culture supernatant,Western blotting was used to detect the expression of Nrf2,HO-1 and NQO1.Real time RT-PCR was used to detect the expression of Nrf2,HO-1 and NQO1 after ICA addition for 2,6 and 24 h.And immunofluorescence was used to observe the activation of Nrf2.RESULTS ICA reduced LPS-induced NO,IL-1β and IL-18 production in the culture supernatant,and ICA increase LPS-induced mRNA and protein expression of Nrf2 signaling pathway.CONCLUSION ICA protects LPS induced neuroinflammation by regulating Nrf2 signaling pathway.
文摘OBJECTIVE Astroglia support neurons by providing substrates for neuronal metabolism, glutamate clearance and anti-oxidant protection. Nuclear factor erythroid 2-related factor 2(Nrf2) is the main switch of intracellular antioxidant defense system. Also, Nrf2 signaling is recognized to activate the neurotrophic pathway to replace/protect damaged organelles. Ellagic acid(EA), an excretion component of fruits and nuts, displays anti-oxidant, cardioprotective and antiinflammatory activities. However, few studies have been focused on the neurotrophic properties of EA. Our study investigated whether EA could enhance astroglia neurotrophic effects to support neurons and the underlying mechanisms as well. METHODS Primary neuron-enriched cultures, primary astroglia-enriched cultures and primary neuron-astroglia co-cultures were applied to detect whether pharmacological regulation of astroglia function by EA could be utilized to overcome neuronal death. RESULTS This study indicated that EA promoted neuronal survival. Furtherly, astroglia Nrf2 participate in EA-elicited neuronal survival with the following scenarios. First, EA induced astroglia proliferation, neurotrophic factors release and Nrf2 activation. Second, astroglia-targeted Nrf2 si RNA inhibited EA-mediated astrogliosis,neurotrophic factors excretion and neuronal survival. CONCLUSION EA mediated astroglia Nrf2 activation to enhanced neurotrophic effects on neurons, and these findings might provide new strategies for neurotrophic factor-based treatment of neurodegenerative disease.
