Sodium butyrate aids brain injury repair in neonatal rats

TL;DR

Sodium butyrate helps repair brain injuries in newborn rats by improving gut health and reducing inflammation.

Contribution

This study reveals a novel mechanism by which sodium butyrate aids brain injury repair through gut microbiota modulation and inflammation regulation.

Findings

SB reduced intestinal and brain injuries in neonatal rats with NEC and HIBI.

SB increased IL-10 and decreased IL-17 levels, indicating reduced inflammation.

SB improved gut microbiota diversity and regulated Bcl-2 and Bax expression in tissues.

Abstract

The aim of this study is to investigate the effects and mechanism of action of sodium butyrate (SB) on brain injury repair in neonatal rats. 126 neonatal SD rats were randomly allocated to 7 groups, and necrotizing enterocolitis (NEC) and hypoxic–ischemic brain injury (HIBI) rat models were established. Hematoxylin and eosin staining showed that SB intervention alleviated intestinal and brain injuries in the HIBI + SB, NEC + SB, and NEC + HIBI + SB groups. Compared to the NEC and NEC + HIBI groups, the NEC + SB and NEC + HIBI + SB groups had significantly higher interleukin (IL)-10 and lower IL-17 levels (P < 0.05). Immunohistochemistry revealed increased Bcl-2 expression and decreased Bax expression in the NEC + SB and NEC + HIBI + SB groups compared to the NEC and NEC + HIBI groups in intestinal and brain tissues (P < 0.05). Compared to the control group (CG), gut microbiota diversity decreased in the HIBI, NEC, and NEC + HIBI groups, and increased significantly in the HIBI + SB, NEC + SB, and NEC + HIBI + SB groups. SB may alleviate brain injury by modulating gut microbiota, affecting IL-10 and IL-17 levels, and regulating Bcl-2 and Bax expression in intestinal and brain tissues.

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