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首页> 外文期刊>Neuroreport >Upregulation effects of Tanshinone IIA on the expressions of NeuN, Nissl body, and I kappa B and downregulation effects on the expressions of GFAP and NF-kappa B in the brain tissues of rat models of Alzheimer's disease
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Upregulation effects of Tanshinone IIA on the expressions of NeuN, Nissl body, and I kappa B and downregulation effects on the expressions of GFAP and NF-kappa B in the brain tissues of rat models of Alzheimer's disease

机译：丹参酮IIA对阿尔茨海默病模型大鼠脑组织NeuN，Nissl体和IκB表达的上调作用以及对GFAP和NF-κB表达的下调作用

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This study aimed to observe the effects of Tanshinone IIA(Tan IIA) treatment on the expression levels of brain tissue NeuN, Nissl body, IB, GFAP and NF-B in Alzheimer's disease (AD) rats to explore the possible anti-inflammatory and neuroprotective mechanisms of Tan IIA. Thirty healthy male Sprague-Dawley rats were randomized into three groups: Sham group, AD+vehicle control group, and AD+Tan IIA group. The models of AD were established by injecting A1-42 into the hippocampus of rats. Tagged position and the expression levels of A1-42 were observed by immunohistochemistry staining to prove the success of the model of AD. Brain tissues of all groups were collected after Tan IIA treatment and paraffin sections were prepared to assess pathological changes and expression levels of GFAP, IB and NF-B by both immunohistochemistry and western blotting. After A1-42 injection, the expression levels of GFAP and NF-B were significantly stronger in the AD+vehicle control group than those in the AD+Tan IIA group and the sham group (P<0.05), the IB expression level and the number of neurons and Nissl bodies of AD+vehicle control group was reduced compared with the sham or the AD+Tan IIA group (P<0.05). In conclusion, A induces a cerebral tissue inflammation reaction. Tan IIA treatment can suppress the proliferation of astrocytes in an AD model, lower the level of NF-B, and increase the level of NeuN, Nissl body, IB, thus exerting anti-inflammatory and neuroprotective effects.
机译：本研究旨在观察丹参酮IIA（Tan IIA）处理对阿尔茨海默病（AD）大鼠脑组织NeuN，Nissl体，IB，GFAP和NF-B表达水平的影响，以探讨可能的抗炎和神经保护作用Tan IIA的机制。将三十只健康的雄性Sprague-Dawley大鼠随机分为三组：假手术组，AD +车辆对照组和AD + Tan IIA组。通过将A1-42注射到大鼠海马中来建立AD模型。免疫组化染色观察标记位置和A1-42表达水平，证明AD模型成功。 Tan IIA处理后收集所有组的脑组织，并准备石蜡切片以通过免疫组织化学和蛋白质印迹来评估GFAP，IB和NF-B的病理变化和表达水平。注射A1-42后，AD +车辆对照组的GFAP和NF-B的表达水平显着高于AD + Tan IIA组和假手术组（P <0.05），IB的表达水平和假手术组。与假手术组或AD + Tan IIA组相比，AD +车辆对照组的神经元和Nissl体数量减少（P <0.05）。总之，A引起脑组织炎症反应。 Tan IIA治疗可以抑制AD模型中星形胶质细胞的增殖，降低NF-B的水平，并增加NeuN，Nissl体，IB的水平，从而发挥抗炎和神经保护作用。

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