alleviates adenine-induced acute kidney injury in mice by improving intestinal barrier function

Acute kidney injury (AKI) is a kind of critical kidney disease characterized by tubular injury, rapid decline of renal function and renal inflammation, with high clinical incidence. AKI has been shown to be associated with dysregulation of the gut microbiota and impaired intestinal barrier. Bifidobacterium has a positive impact on the treatment of many diseases. However, little is known about the role and mechanism of Bifidobacterium in AKI. Based on previous experiments, Bifidobacterium bifidum FL228.1 and FL276.1, which can relieve intestinal inflammation, and Bifidobacterium bifidum ZL.1, which has anti-inflammatory potential, were screened. This study aimed to investigate the effects of Bifidobacterium bifidum FL228.1, FL276.1 and ZL.1 on AKI, focusing on their role in the gut microbiota composition and intestinal barrier function. Our results showed that Bifidobacterium bifidum FL228.1, FL276.1 and ZL.1 effectively improved kidney function in mice with AKI by regulating the gut microbiota dysregulation, inhibiting intestinal inflammation and rebuilding the intestinal mucosal barrier. In addition, intervention with probiotics turned the gut microbiota disturbance caused by AKI into a normalized trend, reversed the adverse outcome of microbiota imbalance, and increased the abundance of potentially beneficial bacteria Bifidobacterium and Faecalibaculum . In summary, Bifidobacterium bifidum FL228.1, FL276.1, and ZL.1 alleviate adenine-induced AKI based on the gut-kidney axis. Although their mechanisms of action are different, their effect on alleviating AKI is almost the same. Bifidobacterium bifidum FL228.1, FL276.1 and ZL.1 effectively improved kidney function in mice with AKI by regulating the gut microbiota dysregulation, inhibiting intestinal inflammation and rebuilding the intestinal mucosal barrier.