摘要目的:观察消退素D1(RvD1)对急性肺损伤小鼠肺部炎症反应和Nod样受体蛋白3(NLRP3)炎性小体表达的影响。方法:体质量25～30 g的BALB/c小鼠30只分为3组(各10只)，正常对照组鼠尾静脉注射等体积9 g/L盐水；脂多糖(LPS)组小鼠尾静脉注射LPS(10 mg/kg)，作用6 h；RvD1组小鼠注射LPS 30 min前予RvD1(5 μg/kg)尾静脉注射，LPS作用6 h。观察各组小鼠肺组织病理学改变，肺部炎性因子白细胞介素-18(IL-18)、白细胞介素-1β (IL-1β)及NLRP3炎性小体的表达改变。结果:LPS组小鼠经LPS刺激后，小鼠肺组织出现病理损伤，炎性因子IL-18、IL-1β水平均较正常对照组小鼠明显升高，差异均有统计学意义(均 P<0.05)，肺组织NLRP3、凋亡相关点样蛋白(ASC)及半胱氨酸天冬氨酸蛋白酶-1(Caspase-1)表达较正常对照组小鼠明显升高，差异均有统计学意义(均 P<0.05)。RvD1组小鼠予RvD1预处理后，肺组织病理损伤减轻，炎性因子IL-18、IL-1β水平较LPS组均明显降低，差异均有统计学意义(均 P<0.05)；同时RvD1组NLRP3、ASC及Caspase-1表达较LPS组显著降低，差异均有统计学意义(均 P<0.05)。 结论:RvD1能减轻急性肺损伤肺部炎症反应，抑制炎性因子的释放，该效应与抑制NLRP3的表达有关。

abstractsObjective:To investigate the effects of Resolvin D1 (RvD1) on the inflammatory response and the expression of Nod-like receptor protein 3(NLRP3) inflammasomes in mice with acute lung injury.Methods:The 30 male BALB/c mice weighing 25-30 g were divided into 3 groups(each group with 10 mice). Mice in the normal control group were given normal saline by tail vein injection.Mice in the lipopolysaccharide (LPS) group were given the same volume of LPS (10 mg/kg) via tail vein injection.Mice in the RvD1 group were injected with RvD1 (5 μg/kg) through the tail vein 30 minutes prior to LPS administration.Mice were humanely sacrificed after 6 hours.Histopatholo-gical changes of lung tissue, the levels of pro-inflammatory cytokines interleukin(IL)-18 and IL-1β, and the expression of NLRP3 inflammasomes in lung tissue were measured.Results:After LPS administration, the lung of mice showed pathological damage.The levels of pro-inflammatory factors IL-18 and IL-1β as well as the expression of NLRP3, apoptosis-associated speck-like protein containing a card(ASC)and Caspase-1 in the LPS group were significantly higher than those in the normal control group (all P<0.05). After pretreatment with RvD1, the pathological damage of lung tissue was alleviated.The levels of pro-inflammatory factors IL-18 and IL-1β as well as the expression of NLRP3, ASC and Caspase-1 in the RvD1 group were significantly lower than those in the LPS group (all P<0.05). Conclusions:RvD1 can attenuate the pulmonary inflammation in acute lung injury and inhibit the release of pro-inflammatory factors, which is possibly related to the suppression of NLRP3.