Effect of butyrate, a short-chain fatty acid, in repairing brain injury in neonatal rats

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Abstract Butyrate, as a microbial metabolite, is considered to have an effect on improving the intestinal microenvironment. At present, it is shown that the brain and gut interact with each other through the gut-microbiota-immune-brain axis. An aberrant gut-microbiota-immune-brain axis in premature infants may aggravate brain injury. However, whether sodium butyrate can improve the microbial-intestinal-brain axis to repair the brain injury in premature infants remains unclear. In this study, we established a neonatal rat hypoxic-ischemic brain injury model and a necrotizing enterocolitis model. It was found that enteritis could lead to the occurrence and aggravation of brain injury, which might be associated with the increased secretion of inflammatory factor interleukin-17 caused by the down-regulation of suppressor of cytokine signaling 1 (SOCS1). Further studies showed that sodium butyrate can up-regulate the expression of SOCS1, and increase the secretion of anti-inflammatory interleukin-10, which may alleviate the neurological dysfunction caused by brain injury. This study provides a new theoretical basis for further exploration of the mechanism of brain injury repair in premature infants.