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作 者:陶燕燕 梁国庆[1] 蔡伟 王晓静 张芯 牛秀珑 陈少伯 TAO Yan-yan;LIANG Guo-qing;CAI-Wei;WANG Xiao-jing;ZHANG Xin;NIU Xiu-long;CHEN Shao-bo(Institute of Prevention and Treatment of Cardiovascular Diseases in Alpine Environment of Plateau,Characteristic Medical Center of the Chinese People′s Armed Police Force,Tianjin 300162,China)
机构地区:[1]武警部队特色医学中心高原高寒环境及心血管病防治研究所,天津300162
出 处:《医学研究生学报》2020年第8期802-807,共6页Journal of Medical Postgraduates
基 金:国家重点研发计划(2017YFC1307602);天津市科技重大专项(15ZXJZSY00010)。
摘 要:目的舒洛地特与子痫前期等妊娠高血压疾病的关系目前报道较少。文中旨在观察舒洛地特对子痫前期孕期血清诱导下人脐静脉内皮细胞功能损伤的保护作用,并探讨其相关分子机制。方法收集2019年1月至6月武警部队特色医学中心妇产科20份孕12周正常产妇血清(NPS)及20份孕12周子痫前期血清(PES)。以不同浓度舒洛地特(0、0.1、0.3、1、3、10、30 LSU/mL)干预人脐静脉内皮细胞系HUVEC和Ea.hy926。以孕12周的NPS、PES及有效浓度舒洛地特共同干预细胞,分为:对照组(胎牛血清+NaCl)、NPS组(NPS+NaCl)、NPS+0.3 LSU/mL舒洛地特组、NPS+10 LSU/mL舒洛地特组、PES组(PES+NaCl)、PES+0.3 LSU/mL舒洛地特组、PES+10 LSU/mL舒洛地特组。分别用CCK8法和Matrigel法检测细胞增殖和管腔形成能力,并确定舒洛地特的有效浓度。Matrigel法观察舒洛地特对病理血清诱导下内皮功能损伤的保护作用。以ELISA法测定细胞上清液中血管内皮生长因子受体-1(sFLT-1)和胎盘生长因子(PlGF)的分泌水平。结果在HUVEC、Ea.hy926细胞中,NPS+0.3 LSU/mL舒洛地特组sFLT-1表达量较NPS组明显降低(P<0.01),PlGF表达量较NPS组明显升高(P<0.01);PES组sFLT-1表达量较NPS组、PES+0.3 LSU/mL舒洛地特组明显升高[(2653.55±31.24)ng/mL vs(1708.45±38.75)ng/mL,P<0.01]。在Ea.hy926融合细胞中,PES组PlGF表达量较PES+0.3 LSU/mL舒洛地特组明显降低(P<0.01)。结论0.3 LSU/mL舒洛地特可对子痫前期诱导的内皮细胞功能受损产生保护作用,该作用与调节内皮细胞sFLT-1/PIGF的分泌平衡有关。Objective The relationship between glycosaminoglycans sulodexide(SDX)and HDP such as preeclampsia(PE)has not been reported.The purpose of this study is to observe the protective effect and molecular mechanism of SDX on the function damage of human umbilical vein endothelial cells induced by pregnancy serum of PE.Methods the indicated concentrations of SDX(0,0.1,0.3,1,3,10,30 LSU/mL)were used to interfere with HUVEC and Ea.hy926 cells.CCK8 and Matrigel methods were used to detect cell proliferation and tube formation.The normal pregnant women serum(NPS)or PE patients serum(PES)which collected at the 12 th week of pregnancy and the effective concentration of SDX were used to intervene the cells.Matrigel methods were used to observe the protective effect of SDX on endothelial function damage which induced by pathological serum.The secretion level of sFLT-1 and PlGF in supernatant were determined by ELISA.Results Compared with the control group,high concentration of SDX inhibited the proliferation of endothelial cells.SDX significantly promoted the tube formation activity wiht a peak at 0.3 LSU/mL(P<0.01).PES damaged the tube formation activity.0.3 LSU/mL SDX protected cells from tube formation damage which induced by PES(P<0.01).PES promoted the secretion of sFLT-1 and inhibit the secretion of PlGF,while 0.3 LSU/mL SDX reversed the secretion of sFLT-1 and PlGF induced by PES(P<0.01).Conclusion 0.3 LSU/mL SDX can protect endothelial cells from PES induced endothelial dysfunction,which is associated with the secretion balance regulation of sFLT-1/PlGF.
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