Effects Of ω-3 Polyunsaturated Fatty Acids On Intestinal Function And Inflammatory Response In Burned Rats

Objective: To investigate the effects ofω-3 polyunsaturated fatty acids on intestinal mucosa injury and inflammatory responses following severe burn.Method: A total of 72 SD rats with 30% total body surface area(TBSA) full thickness burn were randomly divided into 3 groups: (1) normal control group (A group,n = 8); (2) the experimental group (B group,n = 32) (3).treatment group (C group,n = 32). A group of rats was injected NS with 2 mL / (kg ? d) by tail vein, B,C group of rats was injected 20% middle-long-chain fatty emulsion orω-3 fish oil with 2 mL / (kg ? d) by tail vein at the same time every day.Before injury group (A group) and after injury groups (C group, B group) were measured respectively the levels of serum LPS, IL-6, TNF-α, DAO,observed morphological changes of ileum by normal light and TEM,and detected expression of TNF-α,NF-κBp65 in intestinal tissue by immunohistochemical staining. Each subgroup is 8 rats.Results: 1. Serum LPS, IL-6, TNF-α, DAO was significantly higher than pre-injury at each time point after injury in B, C groups, (P <0.01). The levels in C group were lower than in B group, and were significantly different in 4,7,10 day after injury (P <0.05 or P <0.01). 2. Compared with the B group, TNF-α, NF-κBp65 activity was significantly decreased in C group. 3. TEM observation:Compared with normal rats by TEM, tight junctions structure of intestinal epithelial were damaged, fractured, and cells gap widen, band structure density decreased in B group and C group. The band structure of tight junction of intestinal epithelia were integrated in C group, and density increased.Conclusions: 1.ω-3 PUFAs reduce serum DAO, LPS levels, improve intestinal mucosa injury, and protect the function of intestinal mucosal barrier after burn. 2.ω-3 PUFAs reduce the releasing of pro-inflammatory media,example IL-6, TNF-αto promote immune dysfunction after burn . 3. The possible mechanism ofω-3 PUFAs is reduce the binding rate of nuclear transcription factor (NF-κB) and DNA, block NF-κB signaling pathway, reduce the production of various inflammatory mediators.