Objective To investigate the protective effect of hyperbaric oxygen (HBO) combined with ω-3 polyunsaturated fatty acid (PUFA ω-3) on lipopolysaccharide-induced acute lung injury in the rats and its related mechanism.Methods Forty-eight SD rats were randomly divided into the control group,the model group,the experimental group and the combined group,each consisting of 12 rats.With exception of the rats in the control group,acute lung injury (ALI) model was established by LPS tracheal instillation in the rats of the model and experimental groups.The experimental group received PUFA ω-3 (150 mg/kg) by gavage,the combined group was treated with HBO on the basis of PUFA omega-3,and equal volume of distilled water was given to the control and model groups.The course of treatment lasted for 14 days.After last medication,pulmonary tissues of the rats were collected and wet/dry ratio was calculated,and the inflammatory factors,TNF-α and IL-1β in the lung tissue homogenate were detected by ELISA test kit.HE staining was used to observe the pathological damage of the lung tissue,and the expression levels of TLR4 and NF-κB proteins in the lung tissue were detected by Western-blotting.Results Compared with the control group,pulmonary edema in the model group could clearly be seen,and the wet/dry ratio of the lung tissue increased markedly (5.57 ± 0.57 vs.4.16 ±0.19) (P ＜0.05).Compared with the model group,the wet/dry ratio of the lung tissue in the experimental and the combined groups decreased (4.78 ±0.25,4.42 ±0.18 vs.5.57 ±0.37) (P ＜0.01 or P ＜ 0.05),and the wet/dry ratio of the combined group was obviously lower than that of the experimental group (4.42 ±0.18 vs.4.78 ±0.25) (P ＜0.05).As compared with the control group,the inflammatory factor levels of TNF-α and IL-1β in the model group all significantly increased(P ＜ 0.01 or P ＜ 0.05).Following treatment with simple PUFA ω-3 or coupled with HBO,the inflammatory factor levels of TNF-α and IL-1β in lung tissues of the experimental and the combined groups all decreased markedly,as compared with those of the model group (P ＜ 0.05),with those of the combined group decreased more significantly (P ＜ 0.05).As compared with those of the control group,the expression levels of TLR4 and NF-κB proteins in the model group were significantly up-regulated (P ＜ 0.01).Compared with the model group,the expression levels of TLR4 and NF-κB proteins in the experimental and the combined groups all decreased(P ＜0.01 or P ＜0.05),with the down-regualtion of TLR4 in the experimental group displaying more markedly (P ＜ 0.01).Compared with the experimental group,the down-regulation of NF-κB protein in the combined group was more significant (P ＜ 0.05).Conclusion HBO could obviously enhance the protective effect of PUFA ω-3 on the lung tissue of the rats with ALI and reduce the level of inflammatory factors,which might be associated with the regulation of TLR4/NF-κB signal pathway.

Objective To investigate the protective effect of hyperbaric oxygen (HBO) combined with ω-3 polyunsaturated fatty acid (PUFA ω-3) on lipopolysaccharide-induced acute lung injury in the rats and its related mechanism.Methods Forty-eight SD rats were randomly divided into the control group,the model group,the experimental group and the combined group,each consisting of 12 rats.With exception of the rats in the control group,acute lung injury (ALI) model was established by LPS tracheal instillation in the rats of the model and experimental groups.The experimental group received PUFA ω-3 (150 mg/kg) by gavage,the combined group was treated with HBO on the basis of PUFA omega-3,and equal volume of distilled water was given to the control and model groups.The course of treatment lasted for 14 days.After last medication,pulmonary tissues of the rats were collected and wet/dry ratio was calculated,and the inflammatory factors,TNF-α and IL-1β in the lung tissue homogenate were detected by ELISA test kit.HE staining was used to observe the pathological damage of the lung tissue,and the expression levels of TLR4 and NF-κB proteins in the lung tissue were detected by Western-blotting.Results Compared with the control group,pulmonary edema in the model group could clearly be seen,and the wet/dry ratio of the lung tissue increased markedly (5.57 ± 0.57 vs.4.16 ±0.19) (P ＜0.05).Compared with the model group,the wet/dry ratio of the lung tissue in the experimental and the combined groups decreased (4.78 ±0.25,4.42 ±0.18 vs.5.57 ±0.37) (P ＜0.01 or P ＜ 0.05),and the wet/dry ratio of the combined group was obviously lower than that of the experimental group (4.42 ±0.18 vs.4.78 ±0.25) (P ＜0.05).As compared with the control group,the inflammatory factor levels of TNF-α and IL-1β in the model group all significantly increased(P ＜ 0.01 or P ＜ 0.05).Following treatment with simple PUFA ω-3 or coupled with HBO,the inflammatory factor levels of TNF-α and IL-1β in lung tissues of the experimental and the combined groups all decreased markedly,as compared with those of the model group (P ＜ 0.05),with those of the combined group decreased more significantly (P ＜ 0.05).As compared with those of the control group,the expression levels of TLR4 and NF-κB proteins in the model group were significantly up-regulated (P ＜ 0.01).Compared with the model group,the expression levels of TLR4 and NF-κB proteins in the experimental and the combined groups all decreased(P ＜0.01 or P ＜0.05),with the down-regualtion of TLR4 in the experimental group displaying more markedly (P ＜ 0.01).Compared with the experimental group,the down-regulation of NF-κB protein in the combined group was more significant (P ＜ 0.05).Conclusion HBO could obviously enhance the protective effect of PUFA ω-3 on the lung tissue of the rats with ALI and reduce the level of inflammatory factors,which might be associated with the regulation of TLR4/NF-κB signal pathway.

Objective To explore and analyze the effects of ω-3 polyunsaturated fatty acid(PUFA)on oxidative stress and Toll like receptor-4(TLR4)and tumor necrosis factor alpha(TNF-α)in rats with acute lung injury(ALI)induced by lipopolysaccharide (LPS).Methods 120 healthy adult Wistar rats(clean grade;weight,180-240 g)were randomly divided into control group and ob-servation group,60 rats in each group,rats in the control group were randomly divided into untreated group,6 h group(LPS injec-tion),and 24 h group(LPS injection),20 rats in each group.The rats in the observation group were randomly divided into untreated group,6h group(PUFA+LPS injection),and 24 h group(PUFA+LPS injection),20 rats in each group.The relative expression of Superoxide Dismutase(SOD)before treatment,6 h after treatment and 24 h after treatment,Malondialdehyde(MDA),intercellular cell adhesion molecule-1(ICAM-1),TNF-α,and TLR4 in two groups were observed.Results The difference of SOD levels before and after treatment in the two groups of rats was statistically significant(P<0.05),the difference of SOD levels before treatment in the two groups of rats was not statistically significant(P> 0.05).As the processing time went on,the level of SOD in the two groups of rats decreased,but the decrease of the rats in the observation group was lower than that of the control group,and the difference was statistically significant(P<0.05),the difference of MDA level before and after treatment in two groups of rats was statistically significant(P<0.05).As the processing time went on,The level of MDA in the two groups of rats increased,but the increase of the rats in the observation group was significantly lower than that of the control group,and the difference was statistical-ly significant(P<0.05).The difference of ICAM-1 level before and after treatment in the two groups of rats was statistically signif-icant(P<0.05).As the processing time went on,the levels of ICAM-1 and TNF-alpha in the two groups increased,but the increase of the rats in the observation group was significantly lower than that in the control group,the difference was statistically significant (P<0.05).The relative expression of TLR4 in the lung tissue of the observation group was significantly lower than that of the control group(P<0.05).Conclusion PUFA could effectively reduce the oxidative stress and inflammation in ALI rats induced by LPS,which may contribute to the treatment of ALI.