糖尿病相关干眼很常见,而且是早于糖尿病性角膜病变的一组疾病，涉及的组织包括：角膜神经，泪腺，睑板腺和眼表组织等。其发病机制尚不清楚。糖尿病性周围神经病变能够引起泪腺功能单位(LFU)异常，进而导致泪液分泌减少，这可能是糖尿病人群干眼患病率高于正常人群的主要原因之一。SNAP25作为神经特异性蛋白，能够维持神经末梢可塑性，促进神经细胞和内分泌细胞胞吐，它在其他神经系统疾病发病机制的研究已经开展，但是在糖尿病相关干眼角膜神经中的作用机制尚未见报道。本研究采用智能环境控制系统联合STZ建立糖尿病相关干眼模型，观察干眼临床指标和角膜神经改变，检测SNAP25表达水平，明确SNAP25与糖尿病相关干眼发病的关系，并通过调控SNAP25表达水平明确其对角膜神经的保护作用，以及寻找SNAP25蛋白的上游调控因子，深入探寻糖尿病相关干眼的发病机制，为糖尿病相关干眼的早期预防和治疗提供思路和可能。

Diabetes-related dry eye is a common disease and occurs earlier than diabetic keratopathy which involves corneal nerve injury, lacrimal and meibomian gland dysfunction, ocular surface irregularity, et al. To date, the pathogenesis at the molecular levels of diabetes-related dry eye is not clear. The dysfunction of lacrimal functional unit (LFU), a cause of high prevalence of dry eye in diabetic patients, is closely associated with diabetic peripheral neuropathy, leading to decreases in the quality or quantity change of tear film. SNAP25, a neuro specific protein, maintains the plasticity of nerve endings and promotes the exocytosis of nerve cells and endocrine cells. SNAP25 has been linked to the pathogenesis of other nervous system diseases, but its involvement in corneal sensory nerve dysfunction and diabetic corneal nerves has not been reported. We propose to use an intelligent control environmental system that causes dry eye and STZ to induce diabetes in rats to establish a diabetes-related dry eye model. This model would allow us to evaluate the clinical indicators of dry eye, corneal nerve changes, and the expression level of SNAP25, allowing us to establish the relationship between SNAP25 and dry eye diseases with or without diabetes. Furthermore, this project will explore the upstream regulatory factors and downstream effector of SNAP25 in inducing diabetes-related dry eye. The study may provide insights and possibilities for early prevention and treatment of diabetes-related dry eye.