通心络胶囊对糖尿病周围神经病变小鼠黏附分子的作用及其机制

Effect and Mechanism of Tongxinluo Capsule on Adhesion Molecule in Diabetic Peripheral Neuropathy Mice

目的:观察通心络胶囊对糖尿病周围神经病变小鼠黏附分子的作用并探讨其机制。方法:KK/Upj-Ay小鼠随机分为模型组、通心络高、中、低剂量组(4,2,1 g·kg-1),另设C57BL/6小鼠为对照组。灌胃给药12周,测定运动神经传导速度(MNCV)和感觉神经传导速度(SNCV);流式细胞仪测定血液中细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)含量;实时定量荧光PCR(q PCR)和蛋白质印迹(Western blot)法测定坐骨神经ICAM-1,VCAM-1和核因子-κB(NF-κB)表达。结果:与对照组比较,模型组小鼠MNCV,SNCV明显减慢,血液中ICAM-1,VCAM-1含量显著上升,坐骨神经中ICAM-1,VCAM-1和NF-κB表达均明显升高(P<0.01)。与模型组比较,通心络中、高剂量组小鼠MNCV,SNCV明显增快(P<0.05,P<0.01);血液中ICAM-1,VCAM-1含量显著下降(P<0.05,P<0.01);通心络组坐骨神经中ICAM-1,VCAM-1和NF-κB mRNA和蛋白表达显著下降(P<0.05,P<0.01)。结论:通心络胶囊通过下调NF-κB抑制糖尿病周围神经病变小鼠黏附分子表达,改善糖尿病周围神经病变。

Objective： To investigate the effect of Tongxinluo capsule on adhesion molecule in diabetic peripheral neuropathy KK / Upj-Ay mice and its mechanisms.Method： KK / Upj-Ay mice were randomly divided into model,Tongxinluo low-,middle-and high group（4,2,1g·kg-1）.C57BL/6 mice were selected as control group.Mice were given intragastrically for 12 weeks.Motor nerve conduction velocity（MNCV） and sensory nerve conduction velocity（SNCV） were detected.The content of intercellular adhesion molecule-1（ICAM-1） and vascular cell adhesion molecule-1（VCAM-1） in blood were detected by flow cytometer（FCM）.The expression of ICAM-1,VCAM-1 and nuclear factor kappa B（NF-κB） in sciatic nerve were examined by real time PCR and Western blot.Result： Compared with control group,MNCV and SNCV were slower,ICAM-1 and VCAM-1contents in blood were increased and ICAM-1,VCAM-1 and NF-κB expression in sciatic nerve increased in model group（P〈0.01）.Compared with model group,MNCV and SNCV were faster and ICAM-1 and VCAM-1 contents were decreased in Tongxinluo middle,high group（P〈0.05,P〈0.01）.The expression of ICAM-1,VCAM-1and NF-κB mRNA and protein in sciatic nerve of Tongxinluo group significantly decreased（P〈0.05,P〈0.01）.Conclusion： Tongxinluo capsule ameliorates diabetic peripheral neuropathy via inhibiting adhesion molecule expression in the diabetic peripheral neuropathy mice,and this is due to down-regulating NF-κB.