Effect of omega-3 polyunsaturated fatty acid on lipopolysaccharide-induced acute lung injury in rats

Objective To evaluate the effect of dietary ω-3 polyunsaturated fatty acid (PUFA) supplementation on lipopolysaccharide (LPS)-induced acute lung injury in rats.Methods Totally 58 male SD rats were divided into control group (n =10),model group (n =12),ω-3 PUFA high-dose group (n =12),ω-3PUFA medium-dose group (n =12),and ω-3 PUFA low-dose group (n =12).Seven days before model establishment,rats in the three ω-3 PUFA groups were orally given ω-3 PUFA at 1,0.5,and 0.25 g/kg body weight once per day,respectively,for seven consecutive days.Twenty-four hours after the last administration,all rats except those in the control group were given intravenous injection of LPS (6 mg/kg) at caudal vein to establish the model of acute lung injury.Body temperature was measured at 0,6,and 24 hour.Blood samples were collected from the eye venous plexus for routine blood tests and blood biochemical tests 24 hours after modeling.After the rats were sacrificed,the left lung was harvested for measuring the wet weight and dry weight and calculating the wet/dry weight ratio (W/D).The right lung was harvested for pathological observation under light microscope and calculation of semi-quantitative pathological index (PI).Results Twenty-four hours after modeling,deaths were noted in all groups except the control group.After injection of LPS,rats curled with little movements.At 6 hour,the body temperature was significantly higher in the model group than in the control group [(37.4 ±0.27)℃ vs.(35.9 ±0.05) ℃,P =0.00] ; it was (36.2 ±0.38)℃,(36.3 ±0.30)℃,and (36.3 ± 0.32) ℃ in the ω-3 PUFA high-,medium-,and low-dose groups,which were significantly lower than that in the model group (all P =0.01).The amounts of white blood cells,neutrophils,and lymphocytes increased in the model group,but showing no significant difference compared with the other groups.The serum glutamic oxalacetic transaminase (GOT) and glutamic pyruvic transaminase (GPT) levels were significantly higher in the model group than in the control group [(353 ± 235) U/L vs.(157 ± 55) U/L,P =0.02 ; (141± 103) U/L vs.(54 ±23) U/L,P =0.03] ; the ω-3 PUFA high-dose group had significantly lower GOT and GPT levels than the model group did [(167 ±94) U/L vs.(353 ±235) U/L,P =0.03 ; (63 ±57) U/L vs.(141 ± 103) U/L,P =0.04].The model group had significantly higher lung wet weight [(371 ±38) mg vs.(281 ±24) mg,P=0.01] and W/D value (7.34±1.40 vs.5.41 ±0.84,P=0.01) compared with the control group.Compared with the model group,the W/D value was significantly lower in the ω-3 PUFA high-,medium-,and low-dose groups (6.17 ±0.58,P =0.03; 6.17 ± 0.76,P =0.03; 6.13 ± 1.23,P =0.04).Light microscopy showed that the lung alveoli of the model group presented congestion,obvious expansion,and scattered inflammatory cell infiltration in interstitium,along with significantly increased PI compared with the control group (3.9±0.9 vs.0.0±0.0,P=0.00).The PI value was (2.1 ±0.3),(2.1 ±0.3),and (2.3 ± 0.5) in ω-3 PUFA high-,medium-,and low-dose groups,respectively,all significantly lower than that in the model group (all P =0.01).Conclusions The acute lung injury model could be successful established by intravenous injection of LPS.ω-3 PUFA at different doses can improve the acute lung injury of rats.It is therefore supposed that early enteral administration of ω-3 PUFA can alleviate LPS-induced acute lung injury,although the optimal dosage and timing need further research. Key words: ω-3 polyunsaturated fatty acid ;  Docosahexaenoic acid ;  Eicosapentaenoic acid ;  Lipopolysaccharide;  Acute lung injury