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目的:探讨尤瑞克林对2型糖尿病局灶性脑缺血大鼠的神经保护作用及其可能的机制。方法:制备2型糖尿病大鼠局灶性脑缺血模型,尤瑞克林低、中、高剂量组于造模后30 m in舌下静脉一次性注射尤瑞克林3.50×10-3,8.75×10-3和17.5×10-3PNAU.kg-1,24 h后行神经行为学评分和HE染色,免疫组化SABC染色法测定诱导型一氧化氮合酶(iNOS)的含量。实验另设正常大鼠单纯缺血组、模型组,每组12只大鼠。结果:与正常大鼠单纯缺血组比较,2型糖尿病局灶性缺血模型组大鼠神经行为学评分明显升高(P<0.01),HE染色神经细胞受损明显(P<0.01),脑组织海马iNOS活性明显降低(P<0.01)。与模型组比较,尤瑞克林低、中、高剂量组均不同程度降低神经行为学评分及iNOS活性(P<0.01),改善神经细胞的受损程度(P<0.01),其中以中、高剂量组明显(P<0.05),但中、高剂量组间无明显差异(P>0.05)。结论:2型糖尿病能加重缺血性脑损伤的程度,尤瑞克林对2型糖尿病局灶性脑缺血大鼠具有神经保护作用,其机制可能与降低iNOS的活性,减少神经毒性NO的含量有关。
Objective: To investigate the neuroprotective effect of uracil on type 2 diabetic rats with focal cerebral ischemia and its possible mechanism. Methods: Focal cerebral ischemia model was established in type 2 diabetic rats. The low, middle and high dose of uracil was injected into the sublingual vein 30 m in. The neurobehavioral score and HE staining were used to determine the expression of iNOS after treated with different doses of 8.75 × 10-3 and 17.5 × 10-3 PNAU.kg-1 and 24 h respectively. The expression of iNOS was detected by immunohistochemical SABC staining. Another set of experimental normal ischemia group, model group, each group of 12 rats. Results: Compared with normal ischemia group, neurobehavioral scores of model rats with focal ischemia in type 2 diabetes mellitus were significantly increased (P <0.01), and damage of HE staining nerve cells was significant (P <0.01) The iNOS activity in hippocampus of rats decreased significantly (P <0.01). Compared with the model group, the low, middle and high doses of uracil decreased the neurobehavioral score and iNOS activity (P <0.01), and improved the damage degree of nerve cells (P <0.01) High dose group was significantly (P <0.05), but no significant difference between medium and high dose group (P> 0.05). CONCLUSION: Type 2 diabetes can aggravate the degree of ischemic brain injury. Ureclin has neuroprotective effect on focal cerebral ischemia in type 2 diabetic rats. The mechanism may be related to the decrease of iNOS activity and the decrease of neurotoxicity Content related.