芪归糖痛宁颗粒对糖尿病大鼠坐骨神经糖基化终末产物、聚ADP核糖聚合酶基因表达的影响

发布时间：2019-03-19 14:03

【摘要】：目的探讨芪归糖痛宁颗粒对糖尿病周围神经病变(DPN)的作用机制。方法 SD大鼠65只,随机留取10只为空白对照组,其余55只给予高脂饲料喂养4周后,空腹12h链脲佐菌素(STZ)60mg/kg一次性腹腔注射复制DPN大鼠模型,将42只成模大鼠分为模型组(M组)9只、芪归糖痛宁颗粒高剂量组(QTG高组)、芪归糖痛宁颗粒低剂量组(QTG低组)和甲钴胺片组(J组)组各11只,分别予以相应药物灌胃,空白对照组(Con组)和模型组实验期间予以生理盐水灌胃,疗程12周,实验结束后,分别对大鼠空腹血糖(FPG)、神经传导速度、血清超氧化物歧化酶(SOD)、丙二醛(MDA)、神经生长因子(NGF)水平及坐骨神经糖基化终末产物(AGEs)、聚ADP核糖聚合酶(PARP)基因的表达进行检测。结果治疗后,与模型组(M组)比较,芪归糖痛宁颗粒高(QTG高组)、低剂量(QTG低组)组均能降低糖尿病大鼠血糖[(14.08±3.54)mmol/L、(16.11±2.95)mmol/L比(20.41±2.25)mmol/L,P0.01或P0.05)],改善神经传导速度(49.16±5.37)m/s、(43.76±3.93)m/s比(39.66±3.65)m/s,P0.01或P0.05)],降低血清MDA水平(14.91±1.23)nmol/L、(15.22±0.55)nmol/L比(16.75±1.67)nmol/L,P均0.05)],降低坐骨神经AGEs m RNA的表达(0.572±0.021,0.983±0.013比1.088±0.032,P均0.01),降低PARP m RNA的表达(0.677±0.035、0.829±0.015比1.113±0.024,P0.01);与模型组(M组)比较,芪归糖痛宁颗粒高剂量组升高血清SOD水平(112.87±4.98)U/m L比(97.55±4.93)U/m L,P0.01),升高血清NGF水平[(37.38±4.51)ng/L比(26.06±4.41)ng/L,P0.01)]。结论芪归糖痛宁颗粒通过抑制氧化应激与AGEs、PARP途径的相互作用,从而防治和延缓大鼠糖尿病周围神经病变的发生。
[Abstract]:Objective to investigate the effect and mechanism of Qigitangning granule on diabetic peripheral neuropathy (DPN). Methods Sixty-five SD rats were randomly selected as blank control group. The other 55 rats were fed with high fat diet for 4 weeks. The DPN rat model was induced by intraperitoneal injection of streptozotocin (STZ) 60mg/kg for 12 hours on an empty stomach, and the other 55 rats were fed with high fat diet for 4 weeks. Forty-two model rats were divided into model group (M group, n = 9), high dose group (QTG high group), low dose group (QTG low dose group) and mecobalamin group (J group), 11 rats in each group, and 11 rats in model group (group M), high dose group (group QTG), low dose group (group QTG) and group J (n = 11). The rats in control group (Con group) and model group (model group) were treated with saline for 12 weeks. After the experiment, the nerve conduction velocity of fasting blood glucose (FPG),) was measured in rats, respectively, and the control group (control group) and model group were treated with saline for 12 weeks. The levels of serum superoxide dismutase (SOD), malondialdehyde (MDA), (MDA), nerve growth factor (NGF) (NGF) and the expression of (AGEs), polyADP ribosomal polymerase (PARP) gene in sciatic nerve were detected. Results after treatment, compared with the model group (M group), Qigui Tangtong Ning granule (QTG high group) and low dose (QTG low group) could reduce the blood glucose of diabetic rats [(14.08 卤3.54) mmol/L,]. (16.11 卤2.95) mmol/L ratio (20.41 卤2.25) mmol/L,P0.01, (P 0.05)], improved nerve conduction velocity (49.16 卤5.37) mg / s, (43.76 卤3.93) m / s ratio (39.66 卤3.65) m / s, (P < 0.05), (16.11 卤2.95) / (20.41 卤2.25) mmol/L,P0.01, (P < 0.05). (P0.01 or P0.05), decreased serum MDA level (14.91 卤1.23) nmol/L, (15.22 卤0.55) nmol/L vs (16.75 卤1.67) nmol/L,P)], The expression of AGEs m RNA in sciatic nerve was decreased (0.572 卤0.021, 0.983 卤0.013 vs 1.088 卤0.032, P < 0.01), and the expression of PARP m RNA was decreased (0.677 卤0.035, 0.829 卤0.015 vs 1.113 卤0.024, P0.01). Compared with the model group (M group), the high level of serum SOD in the high dose group was significantly higher than that in the model group (112.87 卤4.98 U / L vs (97.55 卤4.93) U / L, P0.01). The serum NGF level increased [(37.38 卤4.51) ng/L vs (26.06 卤4.41) ng/L,P0.01]. Conclusion Qigitangning granule can prevent and delay the development of diabetic peripheral neuropathy in rats by inhibiting the interaction between oxidative stress and AGEs,PARP pathway.
【作者单位】：杭州市余杭区中医院内分泌科;安徽中医药大学第一附属医院内分泌科;
【基金】：基金项目:国家中医药管理局中医药重点学科——内分泌学(No.20091221)
【分类号】：R285.5

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