首页> 美国卫生研究院文献>Environmental Health and Preventive Medicine >The effects of Ginkgo biloba extract (GBe) on axonal transport microvasculature and morphology of sciatic nerve in streptozotocin-induced diabetic rats
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The effects of Ginkgo biloba extract (GBe) on axonal transport microvasculature and morphology of sciatic nerve in streptozotocin-induced diabetic rats

机译:银杏叶提取物(GBe)对链脲佐菌素致糖尿病大鼠轴突运输微血管和坐骨神经形态的影响

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摘要

To evaluate the protective effects ofGinkgo biloba extract (GBe) which has antioxidant activity against peripheral neuropathy due to diabetes mellitus, slow axonal transport and morphology of sciatic nerve including endoneurial microvessels were examined in 12 rats with diabetes mellitus induced by streptozotocin (STZ, 60mg/kg, b.w., i.p.). Six of the diabetic rats were treated with 0.1 % of GBe for 6 weeks from one week after the STZ injection. Serum glucose and lipid peroxide levels in GBe-treated diabetic rats were significantly lower than those in untreated diabetic rats (p<0.01, respectively), though the serum glucose level was higher than that in the control rats. L-[35S] methionine pulse radiolabeling with subsequent gel fluorography demonstrated that mean velocities (Vmean) of actin and β-tubulin, i.e. slow component b (SCb) transport in untreated diabetic rats were significantly lower than those in control rats (p<0.05, respectively); mean diameter of axons in the former rats was significantly smaller than that in the latter (p<0.01). Vmean of actin transport in GBe-treated diabetic rats was significantly faster than that in untreated diabetic rats (p<0.05). Vmean of slow axonal transport was significantly correlated with mean diameter of axons in the three groups of rats combined (p<0.01). On electron microscopy, severe altered endoneurial microvessels decreasing in luminal area together with endothelial cell degeneration or hypertrophy, pericyte debris and basement membrane thickening were observed in untreated diabetic rats; on the other hand these findings were less prominent in the diabetic rats treated with GBe. It is suggested that GBe treatment may protect disturbed slow axonal transport and pathological alterations of peripheral nerve with abnormal endoneurial microvasculature from diabetes mellitus by antioxidant activity.
机译:为了评估对糖尿病引起的周围神经病变具有抗氧化活性的银杏叶提取物(GBe)的保护作用,在链脲佐菌素(STZ,60mg /千克,体重,ip)。从STZ注射后的一周起,六只糖尿病大鼠用0.1%的GBe治疗6周。 GBe治疗的糖尿病大鼠的血清葡萄糖和脂质过氧化物水平显着低于未治疗的糖尿病大鼠(分别为p <0.01),尽管血清葡萄糖水平高于对照组。 L-[ 35 S]甲硫氨酸脉冲放射标记及随后的凝胶透视显示,肌动蛋白和β-微管蛋白的平均速度(Vmean),即未经治疗的糖尿病大鼠中慢速组分b(SCb)的转运显着低于对照大鼠中的那些(分别为p <0.05);前者大鼠的轴突平均直径显着小于后者(p <0.01)。 GBe治疗的糖尿病大鼠中肌动蛋白转运的Vmean明显快于未治疗的糖尿病大鼠中(p <0.05)。在三组大鼠中,轴突缓慢运输的Vmean与轴突的平均直径显着相关(p <0.01)。在电子显微镜下,未治疗的糖尿病大鼠观察到严重改变的神经内膜微血管腔面积减少,以及内皮细胞变性或肥大,周细胞碎片和基底膜增厚。另一方面,这些发现在用GBe治疗的糖尿病大鼠中不那么明显。提示GBe治疗可通过抗氧化作用保护糖尿病引起的神经内膜微血管异常的周围神经的缓慢轴突运输和病理改变。

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