發(fā)布時間：2019-03-19 14:03

【摘要】：目的探討芪歸糖痛寧顆粒對糖尿病周圍神經(jīng)病變(DPN)的作用機制。方法 SD大鼠65只,隨機留取10只為空白對照組,其余55只給予高脂飼料喂養(yǎng)4周后,空腹12h鏈脲佐菌素(STZ)60mg/kg一次性腹腔注射復制DPN大鼠模型,將42只成模大鼠分為模型組(M組)9只、芪歸糖痛寧顆粒高劑量組(QTG高組)、芪歸糖痛寧顆粒低劑量組(QTG低組)和甲鈷胺片組(J組)組各11只,分別予以相應藥物灌胃,空白對照組(Con組)和模型組實驗期間予以生理鹽水灌胃,療程12周,實驗結束后,分別對大鼠空腹血糖(FPG)、神經(jīng)傳導速度、血清超氧化物歧化酶(SOD)、丙二醛(MDA)、神經(jīng)生長因子(NGF)水平及坐骨神經(jīng)糖基化終末產(chǎn)物(AGEs)、聚ADP核糖聚合酶(PARP)基因的表達進行檢測。結果治療后,與模型組(M組)比較,芪歸糖痛寧顆粒高(QTG高組)、低劑量(QTG低組)組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)],改善神經(jīng)傳導速度(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)],降低坐骨神經(jīng)AGEs m RNA的表達(0.572±0.021,0.983±0.013比1.088±0.032,P均0.01),降低PARP m RNA的表達(0.677±0.035、0.829±0.015比1.113±0.024,P0.01);與模型組(M組)比較,芪歸糖痛寧顆粒高劑量組升高血清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)]。結論芪歸糖痛寧顆粒通過抑制氧化應激與AGEs、PARP途徑的相互作用,從而防治和延緩大鼠糖尿病周圍神經(jīng)病變的發(fā)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 鹵3.54) mmol/L,]. (16.11 鹵2.95) mmol/L ratio (20.41 鹵2.25) mmol/L,P0.01, (P 0.05)], improved nerve conduction velocity (49.16 鹵5.37) mg / s, (43.76 鹵3.93) m / s ratio (39.66 鹵3.65) m / s, (P < 0.05), (16.11 鹵2.95) / (20.41 鹵2.25) mmol/L,P0.01, (P < 0.05). (P0.01 or P0.05), decreased serum MDA level (14.91 鹵1.23) nmol/L, (15.22 鹵0.55) nmol/L vs (16.75 鹵1.67) nmol/L,P)], The expression of AGEs m RNA in sciatic nerve was decreased (0.572 鹵0.021, 0.983 鹵0.013 vs 1.088 鹵0.032, P < 0.01), and the expression of PARP m RNA was decreased (0.677 鹵0.035, 0.829 鹵0.015 vs 1.113 鹵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 鹵4.98 U / L vs (97.55 鹵4.93) U / L, P0.01). The serum NGF level increased [(37.38 鹵4.51) ng/L vs (26.06 鹵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.
【作者單位】： 杭州市余杭區(qū)中醫(yī)院內(nèi)分泌科;安徽中醫(yī)藥大學第一附屬醫(yī)院內(nèi)分泌科;
【基金】：基金項目:國家中醫(yī)藥管理局中醫(yī)藥重點學科——內(nèi)分泌學(No.20091221)
【分類號】：R285.5

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