Abstract
Diabetic nephropathy, primarily caused by advanced glycation end products (AGEs), is a serious complication resulting from type 2 diabetes mellitus (T2DM). Reportedly, theaflavins (TFs) can improve diabetic nephropathy; however, the underlying molecular mechanism is not fully clear. In this study, T2DM mice were treated with different concentrations of TFs by gavage for 10 weeks to investigate the effect of TFs on diabetic nephropathy and their potential molecular mechanism of action. Biochemical and pathological analysis showed that the TFs effectively improved blood glucose, insulin resistance, kidney function, and other symptoms in diabetic mice. The mechanism studies indicated that TFs inhibited the formation of AGEs, thereby inhibiting the activation of the MAPK/NF-κB signaling pathway. Therefore, our study suggested that TFs improved diabetic nephropathy by inhibiting the formation of AGEs.