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作 者:郑兴昊 李清 沈锋 杨贵霞 李想 肖川 ZHENG Xinghao;LI Qing;SHEN Feng;YANG Guixia;LI Xiang;XIAO Chuan(Department of Intensive Care Unit,the Affiliated Hospital of Guizhou Medical University,Guiyang 550004,China;Department of Anesthesiology,the Second Affiliated Hospital of Guizhou University of Traditional Chinese Medicine,Guiyang 550002,China;不详)
机构地区:[1]贵州医科大学附属医院重症医学科,贵阳550004 [2]贵州中医药大学第二附属医院麻醉科,贵阳550002
出 处:《实用医学杂志》2022年第24期3032-3036,共5页The Journal of Practical Medicine
基 金:国家自然科学基金(编号:82160365);贵州省卫生健康委科学技术项目(编号:gzwkj2021-034);贵州医科大学国家自然科学基金培育项目(编号:gyfynsfc[2020]-9)。
摘 要:目的观察大黄素(Emodin,ED)对脂多糖(LPS)刺激下肺泡Ⅱ型上皮细胞(AECⅡ)表达促凝和纤溶抑制因子的调节作用。方法将细胞分别给予不同剂量ED(0.25、0.5、1μg/mL)处理1 h后再给予LPS刺激培养24 h。检测细胞中组织因子途径抑制剂(TFPI)、组织因子(TF)、纤溶酶原激活物抑制剂-1(PAI-1)的表达和细胞上清液中Ⅲ型前胶原肽(PⅢP)、凝血酶-抗凝血酶复合物(TAT)、抗凝血酶Ⅲ(AT-Ⅲ)、活化蛋白C(APC)水平。结果LPS刺激后细胞中TF、PAI-1的表达明显增加,TFPI表达明显减少;同时细胞上清液中PⅢP、TAT水平显著增加,AT-Ⅲ、APC水平显著减少。ED剂量依赖性降低了TF、PAI-1的表达,促进了TFPI表达(均P<0.05);同时ED也剂量依赖性逆转了细胞上清液中PⅢP、TAT、AT-Ⅲ及APC水平的变化。免疫荧光提示LPS促进细胞核中p65表达,但这一现象被ED明显抑制。结论ED剂量依赖性地抑制LPS刺激下AECⅡ细胞促凝和纤溶抑制相关因子的表达及分泌,其作用可能与其抑制NF-κB信号通路活化有关。Objective To observe the regulatory effect of emodin(ED)on the expressions of procoagulant and fibrinolysis inhibitory factors in alveolar epithelial cells type Ⅱ(AECⅡ)under LPS stimulation.Methods Cells were given different doses of ED(0.25,0.5,1μg/mL)treated for 1h and then stimulated with LPS for 24 h.The expressions of TF,TFPI,PAI-1 in the cells and the levels of PⅢP,TAT,AT Ⅲ and APC in the cell supernatant were detected.Results The expressions of TF and PAI-1 in LPS stimulated cells significantly increased,while the expression of TFPI decreased.At the same time,the levels of PⅢP and TAT in the supernatant of cells increased,while the levels of AT Ⅲ and APC decreased,which all were reversed by ED in a dose-dependent manner.Immunofluorescence suggested that LPS promoted the expression of p65 in nucleus,which was significantly inhibited by ED.Conclusion ED,in the dose-dependent method,inhibits the expression and secretion of procoagulant and fibrinolytic inhibition factors in AECⅡ cells stimulated by LPS,which may be related to its inhibition of NF-κB signal pathway.
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