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目的:糖尿病周围神经病变的发病机制目前尚不清楚,缺乏特效的治疗方法。本实验拟观察SF对买验性糖尿病神经病变的作用。方法:腹腔注射链脲佐菌素建立糖尿病大鼠模型。糖尿病动物给予黄腐酸钠治疗6个月。测定大鼠的血糖、糖化血红蛋白、热痛缩腿反应潜伏期、神经山梨醇含量,神经组织的光镜及电镜。结果:(1)糖尿病动物血糖明显增高,黄腐酸钠未影响糖尿病动物血糖。(2)黄腐酸钠治疗组热痛缩腿反应潜伏期(7.56±0.46秒)较未治疗的糖尿病组(6.43±0.48秒)明显升高(P<0.05);黄腐酸钠治疗组神经山梨醇(163.45±13.24nmol/mgpr)明显低于未治疗组(279.03±63.37nmol/mgpr)(P<0.05),接近正常组水平(152.60±26.50nmol/mgpr)(P>0.05)。(3)黄腐酸钠治疗组有髓神经纤维密度(11 315.78±1 233.80个/mm~2)明显高于未治疗组(10 140.74±1 237.48个/mm~2)(P<0.05),但尚低于正常组(12 730.55±947.51个/mm~2)(P<0.05)。神经纤维、神经内膜毛细血管的超微结构改变黄腐酸钠组较未治疗组明显减轻。结论:以上结果提示黄腐酸钠可一定程度地抑制实验性糖尿病周围神经病变的进展。
Objective: The pathogenesis of diabetic peripheral neuropathy is not yet clear, the lack of special treatment. The experiment to observe the effect of SF on experimental diabetic neuropathy. Methods: Diabetic rats were induced by intraperitoneal injection of streptozotocin. Diabetic animals were given sodium fulvate for 6 months. The blood glucose, glycosylated hemoglobin, reaction latency of heat shrinking legs, content of neural sorbitol, light microscope and electron microscope of nerve tissue were determined. Results: (1) The blood glucose in diabetic animals was significantly higher, and sodium fulvate did not affect the blood glucose in diabetic animals. (2) Compared with untreated diabetic group (6.43 ± 0.48second), the reaction latency of heat contraction legs (7.56 ± 0.46sec) in sodium fulvate treatment group was significantly higher (P <0.05) The level of alcohol (163.45 ± 13.24nmol / mgpr) was significantly lower than that of the untreated group (279.03 ± 63.37nmol / mgpr) (P <0.05), close to the normal level (152.60 ± 26.50nmol / mgpr) (3) The density of myelinated nerve fibers in the sodium fulvate treatment group (11 315.78 ± 1 233.80 / mm 2) was significantly higher than that of the untreated group (10 140.74 ± 1 237.48 / mm 2) (P <0.05) But still lower than the normal group (12 730.55 ± 947.51 / mm ~ 2) (P <0.05). The ultrastructural changes of nerve fibers and neurofibrillar capillaries were significantly reduced in sodium fulvate group compared with those in untreated group. Conclusion: The above results suggest that fulvic acid can inhibit the progress of experimental diabetic peripheral neuropathy to a certain extent.