Protective Effect of Amygdalin on Acute Kidney Injury Caused by Sepsis

Abstract

Sepsis is a systemic response to infections that may culminate into a life-threatening syndrome, the most common cause of acute kidney injury. Despite increasing mortality associated with septic acute kidney injury, its pathogenesis is poorly understood resulting in limited treatment options. Amygdalin participates in the regulation of various signaling pathways including Janus kinase/signal transducer and activator of transcription 3 signaling pathway. This pathway is critical for initiating immune responses and controlling persistent inflammation in various conditions such as infection. Cecal ligation and puncture is a most frequently used method for modeling sepsis. In the rat cecal ligation and puncture model, the levels of serum creatinine and blood urea nitrogen, as well as the serum levels of proinflammatory cytokines (tumor necrosis factor-α, interleukin-6, and interleukin-18) are significantly elevated. Furthermore, cecal ligation and puncture promotes cell apoptosis with increased BCL2-associated X protein and reduced B-cell lymphoma 2 protein expression. In this study, we have observed amygdalin to reduce serum cytokine secretion and prevent renal cell apoptosis in kidney injury, thus ameliorate kidney injury. The protective role of amygdalin in septic acute kidney injury was mediated through inhibition of Janus kinase/signal transducer and activator of the transcription 3 signaling pathway.