Conclusion
It is a promising domain to explore the multiple pharmacological effects of BBR in AS and metabolic diseases from the perspective of gut microbiota. The research evidence scrutinized herein shows that BBR reverses alterations in the structure, quantity, and composition of gut microbiota under the pathological conditions of AS and metabolic diseases, and induces changes in certain bacterial taxa (Table 1). In addition, BBR improves intestinal barrier function and reduces inflammation in AS and metabolic diseases (Figure 1). Under the pathological conditions of AS and metabolic diseases, increased intestinal permeability has been shown to occur. This promotes systemic inflammation induced by gut microbiota-derived LPS, leading to enhanced IR, IGT, obesity, endothelial dysfunction, and atherosclerotic plaque vulnerability, all of which are ameliorated after BBR treatment. In addition, BBR improves the body’s inflammatory state, glucose and lipid metabolism, and energy homeostasis by regulating gut microbe-dependent metabolites (such as TMAO, SCFAs, BAs, and BCAAs) as well as related downstream pathways, thereby playing a beneficial role in AS and metabolic diseases (Figure 2). It is worth noting that there are still some limitations to existing studies. Although these studies have indicated that BBR alters the gut microbiota of model animals and patients, a direct association between the effect of BBR on gut microbiota and AS and metabolic diseases has not been demonstrated clearly. Moreover, further bacterial transplantation experiments may be needed in the future to provide more direct evidence. More high-quality studies are also needed to explore specific downstream pathways based on the gut microbiota and its metabolites, to better reveal the mechanism of the effect of BBR on AS and metabolic diseases.