The adverse effects of short-term megadose of
antibiotics exposure on the gastrointestinal and liver tissue reactions in young children have been reported.
Antibiotic-induced intestinal and liver reactions are usually unpredictable and present a poorly understood pathogenesis. It is, therefore, necessary to develop strategies for reducing the adverse effects of
antibiotics. Studies on the harm and rescue measures of
antibiotics from the perspective of the gut-liver system are lacking. Here, we demonstrate that
lincomycin exposure reduced
body weight, disrupted the composition of gut microbiota and intestinal morphology, triggered immune-mediated injury and
inflammation, caused
liver dysfunction, and affected lipid metabolism. However,
baicalin administration attenuated the
lincomycin-induced changes. Transcriptome analysis showed that
baicalin improved immunity in mice, as evidenced by the decreased levels of intestinal inflammatory
cytokines and expression of genes that regulate Th1, Th2, and Th17 cell differentiation, and inhibited
mucin type O-
glycan biosynthesis pathways. In addition,
baicalin improved liver function by upregulating the expression of genes involved in
bile acid secretion and
lipid degradation, and downregulating genes involved in
lipid synthesis in
lincomycin-treated mice.
Bile acids can regulate intestinal immunity and strengthen hepatoenteric circulation. In addition,
baicalin also improved anti-inflammatory bacteria abundance (Blautia and Coprobacillus) and reduced pathogenic bacteria abundance (Proteobacteria, Klebsiella, and Citrobacter) in
lincomycin-treated mice. Thus,
baicalin can ameliorate
antibiotic-induced injury and its associated complications such as
liver disease.