乌司他丁对热打击肺泡巨噬细胞TREM-1表达和炎性分泌活性的影响

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目的:探讨乌司他丁对热打击肺泡巨噬细胞TREM-1表达和炎性分泌活性的影响。方法:采集分离10例健康成年男性的肺泡巨噬细胞,分为对照组(Control组)、热打击组(HS组)、乌司他丁低剂量组(HS+LU组)和高剂量组(HS+HU组),每组10例,43℃、5%CO2条件下打击1h,复温培养6h,ELISA检测各组细胞培养上清中肿瘤坏死因子-α(TNF-α)、白介素(IL)-1β和IL-6浓度,流式细胞仪检测细胞中活性氧簇(ROS)水平和细胞表面髓样细胞触发受体-1(TREM-1)表达。结果:HS组、HS+LU组和HS+HU组细胞培养上清中TNF-α、IL-1β和IL-6浓度均高于Control组(P<0.05),而HS+LU组和HS+HU组细胞培养上清中TNF-α、IL-1β和IL-6浓度均低于HS组(P<0.05),其中HS+HU组细胞培养上清中上述炎性递质浓度低于HS+LU组(P<0.05)。HS组、HS+LU组和HS+HU组细胞中ROS水平均高于Control组(P<0.01),而HS+LU组和HS+HU组细胞中ROS水平均低于HS组(P<0.01),其中HS+HU组细胞中ROS水平低于HS+LU组(P<0.01)。HS组和HS+LU组细胞表面TREM-1表达百分比高于Control组(P<0.05),而HS+LU组和HS+HU组细胞表面TREM-1表达百分比均低于HS组(P<0.05),其中HS+HU细胞表面TREM-1表达百分比低于HS+LU组(P<0.01)。结论:热打击可诱导肺泡巨噬细胞TREM-1表达并促进炎性递质分泌,乌司他丁可缓解热打击肺巨噬细胞炎症反应的激活,其潜在机制与调控肺泡巨噬细胞TREM-1表达失衡有关,可能在重症中暑中发挥炎症反应调控作用。 OBJECTIVE: To investigate the effect of ulinastatin on TREM-1 expression and inflammatory secretion in heat-shock alveolar macrophages. Methods: Alveolar macrophages of 10 healthy adult male male were collected and divided into control group, HS group, low dose ulinastatin group (HS + LU group) and high dose group HS + HU group), 10 cases in each group were challenged at 43 ℃ and 5% CO2 for 1 hour and incubated for 6 hours in rewarming culture. The levels of tumor necrosis factor-α (TNF-α), interleukin (IL) ) -1β and IL-6. The level of reactive oxygen species (ROS) and the expression of TREM-1 on the cell surface were detected by flow cytometry. Results: The concentrations of TNF-α, IL-1β and IL-6 in HS +, HS + LU and HS + HU groups were higher than those in Control group (P <0.05) The concentrations of TNF-α, IL-1β and IL-6 in the supernatant of HU group were lower than those in HS group (P <0.05). The concentration of inflammatory mediators in HS + HU group was lower than that in HS + LU group (P <0.05). The levels of ROS in HS, HS + LU and HS + HU groups were higher than those in Control group (P <0.01), while those in HS + LU group and HS + HU group were lower than those in HS group (P <0.01) ). The level of ROS in HS + HU group was lower than that in HS + LU group (P <0.01). The percentage of TREM-1 in HS group and HS + LU group was higher than that in Control group (P <0.05), while the percentage of TREM-1 in HS + LU group and HS + LU group was lower than that in HS group ), In which the percentage of TREM-1 expression on HS + HU cells was lower than that in HS + LU group (P <0.01). CONCLUSION: Thermal shock can induce the expression of TREM-1 in alveolar macrophages and promote the secretion of inflammatory mediators. Ulinastatin can relieve the activation of inflammatory responses induced by thermal shock in pulmonary macrophages. The underlying mechanism is related to the regulation of TREM- 1 expression imbalance, may play an important role in the regulation of inflammatory response in severe stroke.
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