Influence of Resolvin D1 on the inflammatory response and expression of NLRP3 in mice with acute lung injury
10.3760/cma.j.cn101070-20190827-00808
- VernacularTitle:消退素D1对急性肺损伤小鼠肺部炎症反应和Nod样受体蛋白3表达的影响
- Author:
Jun SHI
1
;
Jingxia ZENG
;
Shaodong ZHAO
;
Xiaochen HU
;
Hongjun MIAO
;
Qin ZHANG
Author Information
1. 南京医科大学附属儿童医院重症医学科 210008
- From:
Chinese Journal of Applied Clinical Pediatrics
2020;35(21):1668-1671
- CountryChina
- Language:Chinese
-
Abstract:
Objective: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.