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作 者:唐欣 王修哲 赵玉武[1] TANG Xin;WANG Xiuzhe;ZHAO Yuwu(Department of Neurology,Shanghai Jiao Tong University Affiliated Sixth People’s Hospital,Shanghai 200233,China)
机构地区:[1]上海交通大学附属第六人民医院神经内科,上海200233
出 处:《中风与神经疾病杂志》2021年第6期484-487,共4页Journal of Apoplexy and Nervous Diseases
基 金:国家自然科学基金(31771185);上海市科学技术委员会科研计划项目(17411950103)。
摘 要:目的探讨氧化低密度脂蛋白(ox-LDL)对脑梗死患者巨噬细胞消退素D2(RvD2)合成代谢的影响及其机制。方法收集健康对照组及脑梗死组患者外周血,体外纯化培养巨噬细胞,并将其分为空白对照组和ox-LDL刺激组。比较不同组间巨噬细胞RvD2浓度及15-脂氧酶(15-LOX)、5-脂氧酶(5-LOX)和G蛋白偶联受体18(GPR18)的表达水平,观察巨噬细胞泡沫化程度。结果与空白对照组相比,ox-LDL刺激组的RvD2(P<0.001),15-LOX及GPR18(P<0.05)水平均升高,巨噬细胞泡沫化,但5-LOX在两组间无统计学差异;ox-LDL刺激后,与健康对照组相比,脑梗死组巨噬细胞RvD2增高的绝对值低(P<0.05),巨噬细胞泡沫化程度更严重。结论ox-LDL促进人巨噬细胞保护性合成更高水平的RvD2,其作用机制可能是诱导RvD2合成代谢酶15-LOX的表达;脑梗死患者巨噬细胞保护性合成RvD2功能缺陷。Objective To explore the effects of ox-LDL on the biosynthesis of resolving D2(RvD2)by human periphery blood mononuclear cells(PBMCs)-derived macrophages in ischemic stroke(IS).Methods Matured macrophages were derived from PBMCs of ischemic stroke patients and healthy controls,and were grouped to vehicle group and oxidized low-density lipoprotein(ox-LDL)group.We compared the level of RvD2,15-lipoxygenase(15-LOX)and 5-lipoxygenase(5-LOX),as well as G-protein coupled receptor 18(GPR18).between groups,and determined the formation of foam cells.Results Compared with vehicle group,the level of RvD2(P<0.001),15-LOX and GPR18(P<0.05)in ox-LDL stimulated group was significantly increased,however,no significant difference in the expression of 5-LOX between ox-LDL and vehicle group was observed.After ox-LDL stimulation,compared with healthy control,elevation of RvD2 synthesis in ischemic stroke group was significantly lower(P<0.05),and foam cell formation was also more severe in macrophages of stroke patients.Conclusion Ox-LDL stimulates biosynthesis of RvD2 by human macrophage,perhaps through enhancing 15-LOX expression.Moreover,function of increasing RvD2 synthesis upon ox-LDL stimulation is impaired in stroke patients.
分 类 号:R743.1[医药卫生—神经病学与精神病学]
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