【摘要】 糖尿病性周围神经病变(diabetic peripheral neuropathy,DPN)是最常见的糖尿病慢性并发症之一,其主要临床表现为:麻木、刺痛、痛觉过敏或痛觉超敏。流行病学资料表明,至少有25%的糖尿病患者合并痛性周围神经病变,该疾病严重影响患者的日常生活,已成为重要的社会医疗问题。然而,糖尿病痛性神经病变的发病机制尚不明确,目前的治疗方案非常有限并且疗效欠佳。本文将对该领域研究中糖尿病动物模型的建立,可能的分子机制和临床治疗方案的选择进行综合评述,并重点阐述嘌呤受体可塑性变化及其信号转导通路在糖尿病痛性神经病变中的作用。研究显示,临床常规治疗方法仅能改善患者的部分症状,而根据糖尿病痛性神经病变的病理机制制定的方案,可以对患者进行更全面的治疗。嘌呤受体信号转导通路有望成为治疗糖尿病痛性神经病变的潜在靶点。更多还原

【Abstract】 Diabetic peripheral neuropathy (DPN), one of the most common chronic complications of diabetes, is characterized by al- lodynia, hyperalgesia and spontaneous pain. Chinese epidemiological studies have shown that at least 25% diabetic patients suffered from painful DPN, which compromises patients’ daily functioning and becomes a major health care problem. Although the pathogenesis of painful DPN is not fully understood and current treatment options are very limited, research in the field has advanced our understanding on the mechanism of painful DPN in the past Decade of Pain Research and Control. This review will mainly focus on evaluation of current diabetic animal models, possible molecular pathways and available therapies, with an emphasis on roles of purinergic receptor and its signaling transduction pathways. Common therapies address one or two DPN symptoms, while others offer wider symptom control, presumably by targeting pathophysiological mechanisms of DPN. Purinergic receptor signaling transduction path- ways might become potential targets for treatment for painful DPN.更多还原