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作 者:赵琨 肖云[1] 杨纯 严志凌[2] 董敏娜 向柄全 肖茗耀[1] ZHAO Kun;XIAO Yun;YANG Chun;YAN Zhiling;DONG Minna;XIANG Bingquan;XIAO Mingyao(Dept.of Critical Care Medicine,The 3rd Affiliated Hospital of Kunming Medical University,Kunming Yunnan 650118;Dept.of Gynecological Oncology,The 3rd Affiliated Hospital of Kunming Medical University,Kunming Yunnan 650118;Dept.of Emergency,The 1st Affiliated Hospital of Kunming Medical University,Kunming Yunnan 650032,China)
机构地区:[1]昆明医科大学第三附属医院重症医学科,云南昆明650118 [2]昆明医科大学第三附属医院妇瘤科,云南昆明650118 [3]昆明医科大学第一附属医院急诊医学部,云南昆明650032
出 处:《昆明医科大学学报》2022年第8期41-46,共6页Journal of Kunming Medical University
基 金:云南省科技厅-昆明医科大学应用基础联合专项基金资助项目(202001AY070001-081)。
摘 要:目的探讨白细胞介素-4(IL-4)在急性肺损伤(acute lung injury,ALI)中的保护作用。方法脂多糖(lipopolysaccharide,LPS)诱导A549细胞形成ALI细胞模型。使用不同浓度的IL-4(0.1μg/mL、1μg/mL、10μg/mL)在不同时长下干预该模型,通过流式细胞术检测A549细胞凋亡率,ELISA法测定A549细胞分泌IL-1、IL-6、IL-10、TNF-α、TNF-γ情况。结果IL-4可降低ALI模型中A549细胞凋亡率、抑制Caspase3表达(P<0.05),其效果随IL-4浓度增加及干预时长延长而加强;同时促进Bcl-2表达(P<0.05),IL-4浓度1μg/mL干预12 h时效果最佳。上述条件下,IL-4可降低ALI模型中A549细胞的IL-1、IL-6、TNF-α、TNF-γ,并增加IL-10(P<0.05)。结论IL-4可以通过改善ALI体外模型中细胞因子分泌情况,在急性肺损伤中发挥正向调节作用。Objective To investigate the protective effect of interleukin-4(IL-4)on acute lung injury(ALI).Methods ALI cell models were developed using lipopolysaccharide(LPS)to induce A549 cells.The model was treated with different concentrations of IL-4(0.1μg/mL,1μg/mL,10μg/mL)for different durations.Then the apoptosis rate of A549 cells was detected by flow cytometry,and the secretion of IL-1,IL-6,IL-10,TNF-α,TNF-γof A549 cells was determined by ELISA.Results IL-4 reduced the apoptosis rate of A549 cells and inhibited the expression of Caspase3 in ALI model(P<0.05).The effect was enhanced with the increase of IL-4 concentration and the extension of intervention time.IL-4 promoted the expression of Bcl-2(P<0.05),and the best effect was achieved when the concentration of IL-4 was 1μg/mL for 12 h.Under the above conditions,IL-4 decreased IL-1,IL-6,TNF-α,TNF-γand increased IL-10 in A549 cells in ALI model(P<0.05).Conclusion IL-4 can positively regulate acute lung injury by improving cytokine secretion in ALI in vitro model.
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