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目的：探讨膳食鱼油对感染机体小肠粘膜的保护作用。方法：将大鼠随机分为ＮＳ＋ＣＬＰ，ＦＯ＋ＣＬＰ及ＳＨＡＭ（假手术）三组（ｎ＝１５），术前分别灌食鱼油或等渗盐水１ｍｌ×３周，于ＣＬＰ后第二天采取标本检测血清ＴＮＦ、ＩＬ┐６、ＰＧＥ２浓度及小肠谷氨酰胺（Ｇｌｎ）含量，并用ＲＴ┐ＰＣＲ方法测定小肠粘膜ＴＮＦｍＲＮＡ的含量。结果：ＮＳ＋ＣＬＰ组大鼠血清ＴＮＦ、ＩＬ┐６、ＰＧＥ２水平明显高于ＳＨＡＭ组（Ｐ＜０．０１），小肠粘膜Ｇｌｎ含量显著减少（０．２８±０．１１ｖｓ０．９９±０．２１，Ｐ＜０．０１），而ＴＮＦｍＲＮＡ表达显著升高（Ｐ＜０．０１）。与之相比，灌食ＦＯ大鼠血清ＴＮＦ、ＩＬ┐６、ＰＧＥ２水平则有不同程度的下降，而小肠粘膜Ｇｌｎ含量明显高于ＮＳ＋ＣＬＰ组，同时，小肠粘膜ＴＮＦｍＲＮＡ的表达显著降低（Ｐ＜０．０１）。结论：鱼油能通过抑制花生四烯酸代谢产物的生成，改善小肠粘膜的血循环，或降低粘膜局部细胞因子的表达，阻断细胞因子对肠粘膜结构功能及细胞代谢的不利影响
Objective: To investigate the protective effect of dietary fish oil on the intestinal mucosa of infected mice. Methods: The rats were randomly divided into three groups (n = 15): NS + CLP, FO + CLP and SHAM (n = 15). Fish oil or isotonic saline 1ml × 3 weeks were given before operation. TNF, IL┐6, PGE2 and Gln in small intestine, and the content of TNFmRNA in intestinal mucosa was determined by RT ┐ PCR. Results: Serum levels of TNF, IL┐6 and PGE2 in NS + CLP group were significantly higher than those in SHAM group (P <0.01), Gln in intestinal mucosa was significantly decreased (0.28 ± 0.11 vs 0.99 ± 0.21, P <0.01), while TNFmRNA expression was significantly increased (P <0.01). In contrast, serum TNF, IL┐6 and PGE2 levels in FO rats decreased to some extent, while Gln levels in small intestinal mucosa were significantly higher than those in NS + CLP group (P <0.05) .01). Conclusion: Fish oil can inhibit the formation of arachidonic acid metabolites, improve the blood circulation of small intestinal mucosa, reduce the expression of mucosal local cytokines and block the adverse effects of cytokines on intestinal mucosal structure and cell metabolism