Baicalin Alleviates Short-Term Lincomycin-Induced Intestinal and Liver Injury and Inflammation in Infant Mice

Abstract

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.

Ginsenoside Rg1 Alleviates Ulcerative Colitis in Obese Mice by Regulating the Gut Microbiota–Lipid Metabolism–Th1/Th2/Th17 Cells Axis

“…The reciprocal crosstalk among gut microbiota, lipid metabolism, and Th1/Th2/Th17 cells further amplifies the inflammatory response. 76 For instance, pro-inflammatory cytokines secreted by Th1/Th17 cells can perpetuate dysbiosis, whereas the dysbiotic gut microbiota can promote the polarization of Th1/Th17 cells and impair In our subsequent research, we aim to elucidate the specific mechanisms by which G-Rg1 targets the effector function of Th1/Th2/Th17 cells depending on the gut microbiota. First, we plan to establish a pseudogerm-free mouse model by using antibiotics to clear the gut microbiota.…”

“…Moreover, dysregulated immune responses mediated by Th1/Th2/Th17 cells contribute to the pathogenesis of both UC and obesity. , Th1/Th17 cells secrete IFN-γ, and IL-17A, driving mucosal inflammation in UC, while Th2 cells secrete IL-4 to promote tissue repair. The reciprocal crosstalk among gut microbiota, lipid metabolism, and Th1/Th2/Th17 cells further amplifies the inflammatory response . For instance, pro-inflammatory cytokines secreted by Th1/Th17 cells can perpetuate dysbiosis, whereas the dysbiotic gut microbiota can promote the polarization of Th1/Th17 cells and impair Th2 cell function, exacerbating inflammation and metabolic dysfunction.…”

The Pharmacological Efficacy of Baicalin in Inflammatory Diseases

“…For instance, baicalin (12.5 µM and 25 µM) was found to effectively inhibit the expression of ER stress marker phosphorylated inositol-requiring enzyme 1α (p-IRE1α) and reverse palmitic acid (PA)-induced apoptosis and reactive oxygen species (ROS) production [38]. The main mechanism might be because baicalin reduced PA-induced cytotoxicity by inhibiting ER stress and the activation of thioredoxin-interacting protein (Txnip)/NLRP12 inflammasome [39]. These studies provide a new theoretical basis for the clinical application of baicalin and further improve the cytotoxicity study of baicalin.…”

Exploration of the potential mechanism of Baicalin for hepatic fibrosis based on network pharmacology, gut microbiota, and experimental validation

“…Baicalin (BA) is among the most potent and plentiful flavonoids extracted from Scutellaria baicalensis, and its chemical structure is shown in Figure 1B . Previous studies have shown that BA has antioxidant ( Shi et al, 2018 ), anti-inflammatory ( Zhang et al, 2022 ), anti-apoptosis ( Zhao et al, 2022 ), antiviral ( Zhao et al, 2018 ) and other effects. Recently, there has been an increasing focus on its ability to protect against liver and intestinal tract diseases ( Liao et al, 2020 ).…”

“…Simultaneously, BA may control enteric-related disorders and protect the intestine against sepsis and ulcerative colitis ( Zhu et al, 2020 ). Several trials have also proven BA to alleviate liver disease through the hepatointestinal axis ( Zhang et al, 2022 ).…”