| Background&AimAt the early stage of severe burn injury,scientific and effective intestinal care is an important nursing measure to prevent the occurrence of enterogenous infection and reduce mortality.It has been recognized that the intestinal mucosal barrier dysfunction is the primary cause for bacterial translocation which in turn leads to sepsis and even multiple organ failure in severely burned patients.It has been shown that early enteral nutrition can significantly improve gastrointestinal barrier function,reducing enterogenous infection,sepsis and multiple organ failure following severe burns.However,it is unsatisfied with the implementation of early enteral nutrition because of the high incidence of enteral nutrition intolerance.Therefore,it is of vital importance to explore the nutritional components that effectively protect the intestinal barrier function in patients suffering from enteral nutritional intolerance.Previous studies have shown that severe burns lead to changes in the structure of intestinal flora and a significant decrease in short-chain fatty acids(SCFAs).SCFAs,which mainly include acetate,propionate and butyrate etc,are the products of indigestible polysaccharides produced by intestinal flora fermentation.It has been reported that butyrate has a positive effect on alleviating inflammation by inhibiting histone deacetylases(HDACs)and the release of proinflammatory cytokines.This effect of butyrate has been demonstrated in a variety of intestinal diseases,such as inflammatory bowel disease,celiac disease,irritable bowel syndrome,and colorectal cancer.It has been demonstrated that butyrate,by inhibiting the activation of NODlike receptor family pyrin domain containing protein 3(NLRP3)inflammasome,can protect barrier in intestinal epithelial cell monolayers challenged with lipopolysaccharide.In addition,butyrate,as a nutritional component,can be provided by nurses as a nursing prescription for protecting intestinal barrier funtion.Thus,we hypothesized that butyrate can ameliorate the inflammatory response and secondary injury by inhibiting the activation of NLRP3 inflammasome,consequently protecting the intestinal barrier after severe burns.In this study,we,by utilizing a 30% total body surface area(TBSA)full thickness burned mice model,explore the effects of sodium butyrate supplemented to burned mice on NLRP3 inflammasome activation and intestinal barrier function after severe burns,so as to investigate the underlying molecular mechanisms,which will provide new ideas for resolving the nursing problem of enteral nutrition intolerance.Methods1.A total of 18 healthy female C57 BL / 6 mice were randomly divided into sham burn group,burn group,and burn + sodium butyrate(NaB)group(NaB: 300 mg/kg)respectively.All the mice in both burn group and burn+NaB group were inflicted with 30% TBSA Ⅲ degree scald burn,and observed for 24 h postburn.2.The fluorescein isothiocyanate-dextran fluorescence probe tracing method was used to measure changes in intestinal permeability of mice.3.The intestinal mucosa was stained with hematoxylin-eosin(HE)staining assay,and the histological changes of intestinal mucosa were observed and photographed under light microscope.4.Western blot assay was used to analyze the protein expressions of tight junction(TJ)protein ZO-1,occludin,claudin-1,claudin-2,NLRP3,IL-1βand IL-18 in intestinal mucosa.5.The distribution changes of TJ protein ZO-1 in intestinal mucosa were detected by indirect immunofluorescence assay,and the changes were observed and photographed by laser scanning confocal microscope.Results1.Intestinal permeability was significantly increased in severely burned mice,whereas sodium butyrate significantly reduced the intestinal permeability and ameliorated the disruption of intestinal barrier caused by severe burns.2.The expression of TJ proteins ZO-1,occludin and claudin-1 were significantly decreased,and claudin-2 was remarkably increased in the intestinal mucosa of severely burned mice.However,sodium butyrate significantly increased the proteins expressions of ZO-1 and occludin,and decreased the expression of claudin-2 in the mice suffering from severe burns.3.The distribution of ZO-1 protein in intestinal mucosa was significantly changed after severe burns,whereas sodium butyrate ameliorated the alteration of ZO-1 distribution in intestinal mucosa of severely burned mice.4.Under light microscope,atrophy,edema and inflammatory cell infiltration were observed in the villi of intestinal mucosa from severely burned mice.However,the histological changes of intestinal mucosa in severely burned mice were effectively alleviated by sodium butyrate.5.The protein expressions of NLRP3,IL-1βand IL-18 in intestinal mucosa were significantly increased in severely burned mice,whereas sodium butyrate could significantly reduce the expressions of NLRP3,IL-1βand IL-18 in intestinal mucosa of severely burned mice.Conclusions1.The increase of intestinal permeability caused by severe burns can be significantly reduced by sodium butyrate.Sodium butyrate has a protective effect on intestinal barrier dysfunction induced by severe burn injury.2.Sodium butyrate,by regulating the expressions and distribution of tight junction proteins in intestinal mucosal epithelial cells,plays a protective role in the intestinal barrier function after severe burns.3.Over-activation of NLRP3 inflammasome is involved in the disruption of intestinal barrier function following severe burns.Sodium butyrate protects intestinal barrier function by inhibiting NLRP3 inflammasome activation.4.This study confirmes the protective effect of parenteral sodium butyrate supplementation on the intestinal barrier function,providing a new nutrient for nurses to participate in the protection of intestinal barrier after severe burns,offering a new ingredient to the enteral nutrition research of burn care.It also provides a new direction for improving the nursing intervention about enteral nutrition intolerance. |
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