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作 者:杨光燃[1] 袁申元[1] 朱良湘[1] 袁明霞[1]
机构地区:[1]北京同仁医院微循环糖尿病科,北京100730
出 处:《中国医药导刊》2000年第5期34-36,共3页Chinese Journal of Medicinal Guide
摘 要: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 well known and there is no best therapy. We intended to evaluate the effects of SF on experimental diabetic neuropathy. Methods: Diabetic rats were induced by ip of streptozotocin. Two weeks later, diabetic rats whose plasma glucose is above 16. 6mmol/L were given SF. After six months, plasma glucose, HbAu. , the withdrawal latency caused by thermal stimulation, nerve sorbitol were measured. Nerve pathologic changes were observed by using light and electron microcope. Results: (1) Diabetic rats were hyperglycaemic. There was no effects of SF on hyperglycaemic. (2) The withdrawal latency caused by thermal stimulation was increased in SF - treated group (7. 56±0. 46second), compared to that in untreated diabetes(6. 43±0. 48second). The abnormality in nerve sorbitol was reversed with SF(l63. 45±13. 24nmol/mgpr) ( P < 0. 05) . (3) The myelinated nerve fiber density in untreated group was 10 140. 74 ± 1 237. 48 per mm2, that in SF - treated group was 11 315. 78±1233. 80 per mm2 (P < 0. 05). The ultrastructural changes of nerve fibers and endoneurial capillaries were ameliorated in SF - treated group. Conclusion: These results suggested that SF has a significant effect on the development of experimental diabetc peripheral neuropathy possibly via metabolic and vascular actions.
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