Abstract：
Diabetic distal symmetric polyneuropathy is the most common type of peripheral neuropathy complication of diabetes mellitus. Neuroinflammation is emerging as an important contributor to diabetes-induced neuropathy. Long-term hyperglycemia results in increased production of advanced glycation end products (AGEs). AGEs interact with their receptors to activate intracellular signaling, leading to the release of various inflammatory cytokines. Increased release of inflammatory cytokines is associated with diabetes, diabetic neuropathy, and neuropathic pain. Thus, anti-inflammatory intervention is a potential therapy for diabetic distal symmetric polyneuropathy. Further characterization of inflammatory mechanisms might identify novel therapeutic targets to mitigate diabetic neuropathy.
摘要：
糖尿病远端对称性多发性神经病是糖尿病周围神经病变最常见的并发症。神经炎症正在成为糖尿病引起的神经病变的重要因素。长期高血糖导致晚期糖基化终产物(AGEs)的产生增加。AGEs与其受体相互作用以激活细胞内信号，导致各种炎症细胞因子的释放。炎症细胞因子的释放增加与糖尿病有关，糖尿病神经病变和神经性疼痛。因此，抗炎干预是糖尿病远端对称性多发性神经病的潜在治疗方法.炎症机制的进一步表征可能确定新的治疗靶点以减轻糖尿病性神经病变。
