| 王小军.炎症反应及细胞内钙浓度异常升高在脓毒症发展中的作用分析.[J].中南医学科学杂志.,2020,(2):209-213. |
| 炎症反应及细胞内钙浓度异常升高在脓毒症发展中的作用分析 |
| Inflammatory response and abnormal intracellular calcium concentration in the development of sepsis |
| 投稿时间：2019-06-11 修订日期：2019-11-20 |
| DOI：10.15972/j.cnki.43-1509/r.2020.02.024 |
| 中文关键词: Tlr4 髓质分化蛋白2 NF-κB Stim1 脓毒症 炎症反应 钙超载 |
| 英文关键词:Tlr4 MDP2 NF-κB stim1 sepsis inflammatory response calcium overload |
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| 中文摘要: |
| 探讨炎症反应及细胞内钙浓度异常升高(钙超载)在脓毒症发展中的作用。构建血管内皮细胞损伤模型,后使用基质相互作用分子1(Stim1)抑制表达载体、Tlr4抑制表达载体转染细胞,再通过脂多糖活化Toll样受体4(Tlr4)抑制表达载体转染12 h,脂多糖刺激6 h,使用核转录因子-κB(NF-κB)抑制剂PDTC 以及Tlr4抑制表达载体转染1 h、12 h。结果显示脂多糖刺激人脐静脉内皮细胞后Tlr4、髓质分化蛋白2、NF-κB mRNA相对表达量明显高于刺激前(P<0.05)。Stim1抑制表达载体转染可显著逆转脂多糖诱导的人脐静脉内皮细胞外钙离子内流。Tlr4抑制表达载体+脂多糖组、Tlr4及Stim1抑制表达载体+脂多糖组钙离子浓度明显低于脂多糖组(P<0.05)。 实验表明,下调Tlr4、NF-κB、Stim1表达可显著抑制脂多糖诱导的血管内皮细胞炎症反应和钙超载,缓解脓毒症病情进展。 |
| 英文摘要: |
| To investigate the role of inflammatory reaction and abnormal increase of intracellular calcium concentration in the development of sepsis. Establish vascular endothelial cell injury model. Stim1 was used to inhibit the expression vector and Tlr4 was used to inhibit the expression vector transfected cells. Tlr4 inhibitory expression vector was transfected for 12 hours and lipopolysaccharide stimulated for 6 hours. On the basis of lipopolysaccharide induction. The results showed that the relative expression of TLR4, MDP2 and NF-κB mRNA in human umbilical vein endothelial cells stimulated by LPS was significantly higher than that before stimulation (P<0.05). STIM1 inhibited the extracellular calcium influx induced by LPS. The calcium concentration of TLR4+LPS group, TLR4 and STIM1+LPS group was significantly lower than that of LPS group (P<0.05). The results showed that downregulating the expression of TLR4, NF-κB and STIM1 could significantly inhibit the inflammatory response and calcium overload of vascular endothelial cells induced by lipopolysaccharide, and alleviate the progress of sepsis. |
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