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.
Advanced glycation end products (AGEs), the compounds resulting from the non-enzymatic glycosylation between reducing sugars and proteins, are derived from food or produced de novo. Over time, more and more endogenous and exogenous AGEs accumulate in various organs such as the liver, kidneys, muscle, and bone, threatening human health. Among these organs, bone is most widely reported. AGEs accumulating in bone reduce bone strength by participating in bone structure formation and breaking bone homeostasis by binding their receptors to alter the proliferation, differentiation, and apoptosis of cells involved in bone remodeling. In this review, we summarize the research about the effects of AGEs on bone health and highlight their associations with bone health in diabetes patients to provide some clues toward the discovery of new treatment and prevention strategies for bone-related diseases caused by AGEs.
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