AbstractThe increasing prevalence of depression and diabetes mellitus has become a major public health problem worldwide. Studies have shown that people with diabetes are at a high risk of being diagnosed with depression, and diabetes complicates depression treatment by promoting the deterioration of glycemic control, reducing self-care ability and quality of life, and causing severe functional disability and early mortality. Moreover, health deterioration dramatically increases the financial cost of social and health care system. Thus, how to treat depression, diabetes, and diabetes complicated by depression has become one of the world’s urgent concerns. The activation of nod-like receptor family pyrin domain containing 3 (NLRP3) is closely related to mental illness. This finding provides a new perspective for studying depression. NLRP3 plays an important role in the development of diabetes. In this review, we elaborate the definition and epidemiology of depression, diabetes, and diabetic depression and introduce the functional characteristics of an NLRP3 inflammasome and upstream P2X7 receptor. Moreover, related research on NLRP3 inflammasomes and P2X7 receptors is summarized and used as a reference for confirming that the excessive activation of P2X7- NLRP3 leads to the increased release of inflammatory cytokines, such as IL-1β, in depression and diabetes. We provide insights into the P2X7–NLRP3–IL-1β pathway as an important pathological mechanism and novel therapeutic target in diabetes and depression. Given that the P2X7–NLRP3–IL-1β pathway may play an important role in diabetes confounded by comorbid depression, the possibility of intervention with baicalin is proposed.

中文翻译：

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P2X7 受体介导抑郁症和糖尿病中 NLRP3 炎性体激活

摘要抑郁症和糖尿病的患病率不断上升，已成为全球主要的公共卫生问题。研究表明，糖尿病患者被诊断为抑郁症的风险很高，而糖尿病会促进血糖控制恶化，降低自理能力和生活质量，并导致严重的功能残疾和早期死亡，从而使抑郁症的治疗变得复杂。此外，健康状况恶化极大地增加了社会和医疗保健系统的财务成本。因此，如何治疗抑郁症、糖尿病以及糖尿病并发抑郁症已成为全世界迫切关注的问题之一。 nod样受体家族pyrin结构域3（NLRP3）的激活与精神疾病密切相关。这一发现为研究抑郁症提供了新的视角。 NLRP3在糖尿病的发生发展中发挥着重要作用。在这篇综述中，我们详细阐述了抑郁症、糖尿病和糖尿病抑郁症的定义和流行病学，并介绍了 NLRP3 炎症小体和上游 P2X7 受体的功能特征。此外，还对NLRP3炎症小体和P2X7受体的相关研究进行了总结，作为证实在抑郁症和糖尿病中P2X7-NLRP3的过度激活导致IL-1β等炎症细胞因子释放增加的参考。我们深入了解 P2X7-NLRP3-IL-1β 通路作为糖尿病和抑郁症的重要病理机制和新治疗靶点。鉴于 P2X7-NLRP3-IL-1β 通路可能在合并抑郁症的糖尿病中发挥重要作用，因此提出了黄芩苷干预的可能性。