Background: STAT3, which has moved into mitochondria, is involved in mitochondrial functions such as the respiratory electron transport chain, regulation of cellular metabolism, and scavenging of reactive oxygen species. It is understood that inflammatory bowel disease is known to show damage to intestinal cells and mitochondrial dysfunction due to the inflammatory environment in the intestines. we conducted a study on the amelioration of inflammatory bowel disease through the mitochondrial STAT3 gene.
Methods: We evaluated the potential therapeutic effects the mitochondrial STAT3 gene may exert on inflammtion bowel disease (IBD). The expression of pro-inflammatory cytokines, fibrosis marker and the activity of mitochondria function were examined in intestinal tissues by immunohistochemistry. The microbiomes of mice were analysed using faecal samples.
Results: We observed that the Mitochondrial STAT3 gene improves colitis severity and protects against intestinal destruction. Mitochondrial STAT3 gene reduced INOS and fibosis factors (aSMA, COL1A1), as well as pro-inflammatory cytokines (IL-17, IL-6) in the colon, thereby protecting against colon devastation. Mitochondrial STA3 gene enhanced mitochondria function in colon and immune cell. Furthermore, the beneficial bacteria Lactobacillus reuteri and Akkermansia muciniphila exhibited an increase in the intestinal.
Conclusion: These results suggest that Mitochondrial STAT3 gene ameliorates the severity of experimental colitis, colon mitochondrial function and reduces inflammation through the inhibition of the inflammatory response and necroptosis, offering a potential treatment for UC.