Abstract
Btk has pro-inflammatory role through a variety of signaling pathways. NLRP3 inflammasome plays a central role in liver inflammation for mediating the secretion of pro-inflammatory mediators. However, it is still unknown whether Btk could regulate NLRP3 inflammasome activation in diabetic liver. In this study, we used Btk knockout mice to establish the diabetic model by STZ. We found that Btk knockout could alleviate diabetic liver injury. This protection was due to reduced liver inflammation rather than lipid metabolism. Moreover, we found that macrophage infiltration and pro-inflammatory mediators were both significantly increased in diabetic mice liver. However, Btk deletion could reduce the activation of macrophage and secretion of pro-inflammatory cytokine, and reduced the liver inflammation through suppressing NLRP3 inflammasome activation. In conclusion, our study demonstrated that Btk knockout could significantly attenuate liver inflammation in diabetic mice by down-regulating NLRP3 inflammasome activation. Our finding has a broad prospect and provide a new idea for the treatment of diabetic liver injury.