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目的:应用中药丹参酮(tanshinone IIA,Tan IIA)治疗AD大鼠,观察TanⅡA干预前后,AD大鼠学习记忆、颞叶中诱导型一氧化氮合成酶(iNOS)、基质金属蛋白酶(MMP-2)表达的变化。方法:采用β-淀粉样蛋白(Aβ)定向注射法建立AD大鼠模型,并使用Tan II A干预,通过避暗测试、real-time PCR和Western Blot分别观察大鼠学习记忆能力、大鼠颞叶MMP-2、iNOS两者的mRNA及蛋白表达的变化。应用SPSS13.0进行统计学分析。结果:与假手术组相比,AD组的平均潜伏期缩短(P<0.01),平均错误次数增加(P<0.01),差异均有统计学意义。颞叶内iNOS、MMP-2 mRNA表达均显著增高(P<0.01,P<0.01);两蛋白的表达均显著增高(P<0.01,P<0.01)。与AD组相比,Tan IIA组的平均潜伏期延长(P<0.01),平均错误次数减少(P<0.01),差异均有统计学意义。颞叶内iNOS、MMP-2 mRNA表达均显著下降(P<0.05,P<0.05),两蛋白的表达均显著下降(P<0.01,P<0.01)。结论:Tan II A干预可显著降低AD大鼠颞叶中iNOS、MMP-2 mRNA及蛋白的表达,显著改善AD大鼠的学习记忆能力。其作用机制可能是通过降低Aβ诱导的iNOS及MMP-2的表达,抑制氧化应激损伤来完成。
OBJECTIVE: To observe the effects of TanⅡA on learning and memory, iNOS, MMP-2 in the temporal lobe of Alzheimer’s disease (AD) rats after treatment with TanⅡA (Tan IIA) Changes in expression. Methods: A rat model of Alzheimer’s disease (AD) was induced by β-amyloid (Aβ) -targeting injection. Tan II A was used to observe and study the learning and memory abilities of rats by the dark-avoidance test and real-time PCR and Western Blot. Leaf MMP-2, iNOS both mRNA and protein expression changes. Application SPSS13.0 for statistical analysis. Results: Compared with the sham-operation group, the average latency of AD group was shorter (P <0.01) and the average number of errors was increased (P <0.01). The difference was statistically significant. The expressions of iNOS and MMP-2 mRNA in the temporal lobe were significantly increased (P <0.01, P <0.01), and the expressions of both proteins were significantly increased (P <0.01, P <0.01). The average latency of Tan IIA group was longer than that of AD group (P <0.01), and the average number of errors was decreased (P <0.01). The difference was statistically significant. The expression of iNOS and MMP-2 mRNA in the temporal lobe was significantly decreased (P <0.05, P <0.05), and both proteins were significantly decreased (P <0.01, P <0.01). Conclusion: Tan II A can significantly reduce the expression of iNOS, MMP-2 mRNA and protein in the temporal lobe of AD rats and significantly improve the learning and memory abilities of AD rats. Its mechanism may be through the reduction of Aβ-induced iNOS and MMP-2 expression, inhibition of oxidative stress injury to complete.