ω-3PUFAs、ω-6PUFAs和ω-9MUFAs对LPS诱导急性肺损伤大鼠血清IL-6及细胞凋亡的影响

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目的比较ω-3PUFAs、ω-6PUFAs和ω-9MUFAs三种脂肪乳剂对脂多糖(lipid emulsions,LPS)诱导的急性肺损伤大鼠IL-6分泌的影响。方法 100只大鼠按随机数字分为Control组、LPS组、Intra组、Clino组和Omega组。分别采用生理盐水或不同种类脂肪乳剂处理7d;并均在取标本前8h时于气管内滴入生理盐水或LPS,建立ALI大鼠模型;观察各组大鼠肺组织的病理改变、凋亡指数,测定IL-6mRNA变化以及IL-6蛋白浓度。结果 1)各组大鼠肺组织病理切片均可见明显炎症细胞浸润和出血;2)Clino组和Omega组血清中IL-6mRNA表达较Intra组、LPS组均明显降低;BALF中Clino组和Omega组IL-6蛋白水平明显低于Intra组、LPS组,差异具有统计学意义(P均<0.005)。而Clino组和Omega组两组IL-6mRNA表达及其蛋白水平差异均无统计学意义(P均>0.005)。3)Clino组和Omega组凋亡系数均低于LPS组和Intra组(P均<0.005);Clino组和Omega组AI值差异无统计学意义(P>0.005)。结论 Clinoleic和Omegaven可通过降低IL-6而减轻ALI大鼠炎症反应,并能减轻肺泡上皮细胞凋亡。 Objective To compare the effects of omega-3 PUFAs, omega-6 PUFAs and omega-9 MUFAs on IL-6 secretion in acute lung injury induced by lipopolysaccharide (LPS). Methods 100 rats were randomly divided into Control group, LPS group, Intra group, Clino group and Omega group. Were treated with normal saline or different types of fat emulsion for 7 days. All rats were injected with saline or LPS 8 h before intratracheal instillation to establish ALI model. The pathological changes, apoptosis index , The change of IL-6 mRNA and the concentration of IL-6 protein were measured. Results 1) Inflammatory cell infiltration and hemorrhage were observed in pathological sections of lung tissue of rats in each group. 2) The levels of IL-6 mRNA in serum of Clino group and Omega group were significantly lower than those of Intra and LPS groups. Clino group and Omega group The level of IL-6 protein in LPS group was significantly lower than that in Intra and LPS groups (all P <0.005). However, there was no significant difference in the expression of IL-6 mRNA and protein between Clino group and Omega group (P> 0.005). 3) The apoptosis index in Clino group and Omega group was lower than that in LPS group and Intra group (all P <0.005). There was no significant difference in AI between Clino group and Omega group (P> 0.005). Conclusion Clinoleic and Omegaven can reduce the inflammatory response of ALI rats and decrease the apoptosis of alveolar epithelial cells by decreasing IL-6.
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