Effect Of Sodium Butyrate On Intestinal Injury And Oxidative Stress In Rats With Severe Burn Delayed Resuscitation

1.Background Delayed resuscitation of severe burns often presents with shock,intestinal mucosa due to insufficient effective circulation,causing ischemia and hypoxia injury.After intestinal mucosal injury,bacteria or their toxins in the intestine are easily displaced to cause intestinal infection,which leads to the continued development of shock.Even sepsis and multiple organ dysfunction syndrome(MODS)occur.Therefore,reducing intestinal mucosal damage is one of the keys to prevention of sepsis and MODS.Sodium butyrate is a short-chain volatile fatty acid,an important source of energy for intestinal epithelial cells.In addition,sodium butyrate is a histone deacetylase inhibitor with potential anti-inflammatory and inhibitory effects of inflammatory mediators such as HMGB1,nuclear factor-kappa B(NF-k B),affecting the intestinal barrier,and oxidizing Stress plays an important role.Our previous study demonstrated that sodium butyrate reduced the pulmonary HMGB1 expression,inhibited oxidative stress in the lungs,and alleviated burn-induced acute lung injury.These findings suggest that sodium butyrate may protect against severe burn-induced intestine injury.Therefore,this study used a 30% TBSAⅢ degree burn delayed resuscitation animal model to determine the role of n-butyric acid in delayed intestinal injury and severe oxidative stress changes in the intestine.2.Objective To study the effect of sodium butyrate on intestinal injury and oxidative stress in rats with severe burn delayed resuscitation.3.Materials and Methods Healthy female Sprague–Dawley rats were used throughout the experiment and weighed between 200 grams and 250 grams.All experimental operations were approved by the Animal Experimental Ethics Committee of Anhui Medical University and conducted in accordance with the National Institute of Health’s Guide to Laboratory Animal Care and Use.Prior to the experiment,rats were housed on a standard diet for at least one week and allowed to acclimate to their surroundings,randomly assigned to a sham group(n=8),a burn group(n = 24),burn plus sodium butyrate group(n = 24).After starting the experiment,the rats were anesthetized with 3% sodium pentobarbital(30 mg / kg),shaved on the dorsal side and side,and the constant temperature water bath was set to 98 ℃.After the water was heated to 98 ℃,the burn was burned.Burn group and burn plus sodium butyrate group rats were immersed in water for 12 seconds,then quickly dry the back to avoid additional damage,resulting in 30% TBSA full thickness skin burns.Burn group rats were performed by intraperitoneal injection of 2 ml/kg/TBSA lactated Ringer’s solution at 6,12,and 36 hours after burn.Burns plus sodium butyrate group 400 mg/kg calculated sodium butyrate dose should be used in each rat,then diluted with lactated Ringer’s solution to 1:150,delayed resuscitation by intraperitoneal injection,and Rat lactated Ringer’s solution containing sodium butyrate was administered at the same time point and manner.All the burned rats were sacrificed by blood sampling at 12,24,and 48 hours after scald,and the small intestine tissues were taken out and performed for the histological examination.The concentration of diamine oxidase(DAO)in plasma was determined by ELISA,and the expression of intestinal fatty acid binding protein(IFABP)in intestinal tissues was detected by immunohistochemistry,Detection of MDA and MPO content in intestinal tissue was performed.Rats in the pseudo-burn group were treated with room temperature water to simulate the back scald process without liquid resuscitation,but the same indicators were detected.4.Results Compared with the delayed burn resuscitation group,the DAO concentration in the plasma of delayed burn resuscitation plus sodium butyrate decreased significantly,decreased the expression of intestinal I-FABP and the content of MDA and MPO,and improved the histological changes of intestinal injury induced by delayed resuscitation.5.Conclusion Sodium butyrate can reduce intestinal inflammation and oxidative stress,thereby reducing intestinal damage induced by delayed resuscitation of burns.