Protective effect of dexmedetomidine pretreatment on acute lung injury induced by lipopolysaccharide in rats
Zhouyan Wu, Jiemei Ji, Wan‐Jie Gu, Wenzhi Liu, Jingchen Liu
Abstract
Zhouyan Wu, Jiemei Ji, Wan‐Jie Gu, Wenzhi Liu, Jingchen Liu
Abstract
Objective To investigate the protective effect of dexmedetomidine(Dex) pretreatment on acute lung injury(ALI) induced by lipopolysaccharide (LPS) in rats.Methods A total of 30 male Sprague-Dawley rats were randomly divided into three groups(n=10):control gronp (group C),the LPS group (group L) and the Dex pretreatment group (group D).The rats in the LPS group were intratracheally administered with LPS (5 mg/kg) to duplicate an acute lung injury model.In the group D,the rats were given 50 μg/kg of Dex intraperitoneally 30 min before LPS application.Six hours after LPS administration,arterial blood was drawn for interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) measurement,and the pulmonary tissues were harvested for pathological evaluation,wet/dry (W/D) ratio measurement,biochemical analysis of myeloperoxidase (MPO).Results The Dex pretreatment group compared with LPS group,the levels of wet/dry weight ratio were (4.44±0.08) and (4.76±0.10) respectively (P<0.O1),the levels of MPO activities were (0.70±0.06) and (1.01±0.05) respectively (P<0.01).The value of the oxygen partial pressure in the arteries were (94.0±2.6) mmHg (1 mmHg=0.133 kPa) and (78.0±4.7) mmHg respectively (P<0.05).The levels of TNF-α were (39±9) ng/L and (92±14) ng/L respectively(P<0.05).The levels of IL-6 were (72±16) ng/L and (95±16) ng/L respectively(P<0.05).The pulmonary tissue damage in histopathology in LPS group was more severe than in Dex pretreatment group.Conclusions Dex pretreatment can protect acute lung injury induced by LPS through inhibition of activation of neutrophil in lung tissue and expression of TNF-α and IL-6. Key words: Dexmedetomidine; Lipopolysaccharide; Acute lung injury
A significance statement is not available in the OpenAlex record.
A contribution statement is not available in the OpenAlex record.
Method details are not available in the OpenAlex metadata.
Findings are not separately available in the OpenAlex metadata.
Limitations are not available in the OpenAlex metadata.
Application details are not available in the OpenAlex metadata.
Objective To investigate the protective effect of dexmedetomidine(Dex) pretreatment on acute lung injury(ALI) induced by lipopolysaccharide (LPS) in rats.Methods A total of 30 male Sprague-Dawley rats were randomly divided into three groups(n=10):control gronp (group C),the LPS group (group L) and the Dex pretreatment group (group D).The rats in the LPS group were intratracheally administered with LPS (5 mg/kg) to duplicate an acute lung injury model.In the group D,the rats were given 50 μg/kg of Dex intraperitoneally 30 min before LPS application.Six hours after LPS administration,arterial blood was drawn for interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) measurement,and the pulmonary tissues were harvested for pathological evaluation,wet/dry (W/D) ratio measurement,biochemical analysis of myeloperoxidase (MPO).Results The Dex pretreatment group compared with LPS group,the levels of wet/dry weight ratio were (4.44±0.08) and (4.76±0.10) respectively (P<0.O1),the levels of MPO activities were (0.70±0.06) and (1.01±0.05) respectively (P<0.01).The value of the oxygen partial pressure in the arteries were (94.0±2.6) mmHg (1 mmHg=0.133 kPa) and (78.0±4.7) mmHg respectively (P<0.05).The levels of TNF-α were (39±9) ng/L and (92±14) ng/L respectively(P<0.05).The levels of IL-6 were (72±16) ng/L and (95±16) ng/L respectively(P<0.05).The pulmonary tissue damage in histopathology in LPS group was more severe than in Dex pretreatment group.Conclusions Dex pretreatment can protect acute lung injury induced by LPS through inhibition of activation of neutrophil in lung tissue and expression of TNF-α and IL-6. Key words: Dexmedetomidine; Lipopolysaccharide; Acute lung injury
Key concepts: Lipopolysaccharide, Myeloperoxidase, Dexmedetomidine, Lung, Tumor necrosis factor alpha, Medicine, Internal medicine, Chemistry