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作 者:韩雪妹 王日兴[1] Han Xuemei;Wang Rixing(Department of Emergency,The Second Affiliated Hospital of Hainan Medical University,Haikou 570311,China)
机构地区:[1]海南医学院第二附属医院急诊科,海口570311
出 处:《中华急诊医学杂志》2024年第3期346-352,共7页Chinese Journal of Emergency Medicine
基 金:海南省自然科学基金项目(818MS148);中央引导地方科技发展专项资金(ZY2021HN19)。
摘 要:目的探索IL-22对脂多糖诱导巨噬细胞中NLRP3、caspase-1表达及IL-18、IL-1β分泌的影响。方法体外培养巨噬细胞RAW264.7,将培养的细胞分为3组(空白对照组、LPS组、LPS+IL-22组),并对各组实验细胞进行干预,分别培养3、6、24h,收集各组细胞及上清液,运用RT-PCR、Western Blot、ELISA方法检测巨噬细胞NLRP3炎症小体活化时NLRP3、caspase-1的表达及IL-18、IL-1β的分泌水平。结果单独LPS处理组NLRP3、caspase-1的表达水平升高,IL-18、IL-1β分泌水平均有不同程度的增加,相比对照组差异均有统计学意义;LPS与IL-22共同刺激巨噬细胞后,NLRP3、caspase-1的表达水平,IL-1β、IL-18分泌水平均有不同程度的增加,相比LPS组差异有统计学意义。结论IL-22可增强脂多糖诱导的巨噬细胞中NLRP3、caspase-1的表达及IL-18、IL-1β分泌的,为脓毒症提供新的治疗思路。Objective To explore the effect of interleukin(IL)-22 on the expression of nucleotide binding oligomerization domain like receptor protein 3(NLRP3)and caspase-1 mRNA and secretion of IL-18 and IL-1βin macrophages induced by lipopolysaccharide(LPS),RAW264.7 macrophages were cultured in vitro.Methods Macrophage RAW264.7 was cultured in vitro,and the cultured cells were divided into three groups(control group,LPS group and LPS+IL-22 group),and the experimental cells in each group were intervened,and cultured for 3,6 and 24 h respectively,and the cells and supernatants in each group were collected.RT-PCR,Western Blot and ELISA were used to detect NLRP3 and caspase-1 when the inflammatory body of macrophage NLRP3 was activated.Results The expression levels of NLRP3 and caspase-1 mRNA and the secretion levels of IL-1βand IL-18 were increased in the LPS group,and the differences were statistically significant compared with the control group.After LPS and IL-22 co-stimulated macrophages,the expression levels of NLRP3 and caspase-1 mRNA,and the secretion levels of IL-1βand IL-18 were increased to different degrees,which were significantly increased compared with the LPS group.Conclusion IL-22 could provide a new therapeutic idea for sepsis by enhancing the expression of NLRP3 and caspase-1 mRNA and the secretion of IL-18 and IL-1βin macrophages induced by LPS.
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