Effect of mitochondria-targeted antioxidant SS-31 on sepsis-induced acute lung injury in a mouse model
- VernacularTitle:线粒体靶向抗氧化剂 SS-31肽对脓毒血症小鼠急性肺损伤的影响
- Author:
Guomin LI
;
Dongliang DING
;
Jiaojiao YANG
;
Dong YUAN
;
Jing WU
;
Jianjun YANG
- Publication Type:Journal Article
- Keywords:
Sepsis;
Lung injury;
Oxidative stress;
SS-31
- From:
The Journal of Clinical Anesthesiology
2016;32(5):476-479
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of antioxidant SS-31 on sepsis-induced acute lung injury (ALI)in a mouse model of sepsis.Methods Sepsis was induced in male mice by cecal liga-tion and puncture (CLP).Forty-eight adult male mice (C57BL/6,weight 25-32 g)were equally as-signed to the sham+vehicle group (group A),sham+SS-31 group (group B),CLP+vehicle group (group C),or the CLP+SS-31 group (group D).At 0 or 5 h after CLP or sham operation,mice re-ceived an intraperitoneal injection of SS-31 (5 mg/kg of body weight)or the same volume of normal saline.Pulmonary tumor necrosis factor alpha (TNF-α),interleukin (IL)-6,IL-10,malondialdehyde (MDA),superoxide dismutase activities (SOD),myeloperoxidase activities (MPO ),wet-to-dry weight ratio (W/D),reactive oxygen species (ROS),ATP,NF-κB p65,inducible nitric oxide syn-thase (iNOS),and histological scores were assessed 24 h after operation.Results Pneumonia,edema were significantly heavier in group C than in group A (P <0.05).Lung congestion,inflammatory cell infiltration,alveolar wall edema was significantly less in group D than in group C (P <0.05).Pulmo-nary histological scores,IL-6,MDA,MPO,W/D,ROS,NF-κB p65 and iNOS significantly in-creased,while ATP levels decreased in group C when compared with group A (P <0.05).However, SS-31 treatment significantly reversed these parameters when compared with the group C (P <0.05). No difference was observed between the group A and group B.There was no difference of TNF-α,IL-10,and SOD among the four groups.Conclusion SS-31 improves sepsis-induced ALI in a mouse model probably by down-regulating the oxidative stress and inflammation in of sepsis-induced ALI.
