Introduction: Diabetic peripheral neuropathy (DN) is the most common complication of type 2 diabetes mellitus (T2DM). Objective: This study aimed to explore the role of fibrinogen (FIB) in T2DM neuropathy and its preliminary mechanism. Methods: Ten male Sprague-Dawley rats were divided into a normal control group (NC group) and a T2DM neuropathy model group (DN group). The DN group was given a high-energy diet and streptozotocin, while the NC group was given a normal diet and a citric acid buffer. The expression levels of related proteins were analysed. Results: Electrophysiology: Compared with the NC group, the conduction latency of the somatosensory-evoked potential and nerve conduction velocity was prolonged in the DN group, while the motor nerve action potential was decreased. As seen under a light microscope, the peripheral nerve fibres in the DN group were swollen, and the nerve fibres in the posterior funiculus of the spinal cord were loose or missing. Moreover, as seen under an electron microscope, the peripheral nerve demyelination of the DN group was severe, with microvascular blood coagulation, luminal stenosis, and collapse. Compared with the NC group, in the DN group, the expression of FIB was positively correlated with the expression of both ionised calcium-binding adaptor molecule-1 and glial fibrillary acidic protein. Compared with the NC group, in the DN group, the expression of platelet/endothelial cell adhesion molecule-1 and B-cell lymphoma 2 was negatively correlated. Conclusion: The increased concentration of FIB may be the cause of neuropathy, and its mechanism may be related to its promotion of inflammatory response, blood coagulation, and vascular stenosis.

中文翻译：

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纤维蛋白原在2型糖尿病合并糖尿病神经病变中的作用及其初步机制

简介：糖尿病周围神经病变（DN）是2型糖尿病（T2DM）最常见的并发症。目的：探讨纤维蛋白原（FIB）在T2DM神经病变中的作用及其初步机制。方法：10只雄性Sprague-Dawley大鼠分为正常对照组（NC组）和T2DM神经病变模型组（DN组）。DN组给予高能量饮食和链脲佐菌素，NC组给予正常饮食和柠檬酸缓冲液。分析相关蛋白的表达水平。结果：电生理学：与NC组相比，DN组体感诱发电位和神经传导速度的传导潜伏期延长，运动神经动作电位降低。光镜下可见DN组周围神经纤维肿胀，脊髓后索神经纤维松动或缺失。而且电镜下观察，DN组周围神经脱髓鞘严重，微血管血液凝固，管腔狭窄、塌陷。与NC组相比,DN组FIB的表达量与离子钙结合接头分子1、胶质纤维酸性蛋白的表达量均呈正相关。与NC组相比,DN组血小板/内皮细胞粘附分子1、B细胞淋巴瘤2的表达量呈负相关。结论：FIB浓度升高可能是神经病变的原因，其机制可能与其促进炎症反应、凝血、血管狭窄有关。