丹参酮Ⅱ A 预处理间充质干细胞减轻阿尔茨海默病淀粉样β肽（25-35）诱导的啮齿动物模型的认知功能障碍和氧化应激损伤。
Mesenchymal stem cells after the proprocessing of tanshinone IIA attenuate cognitive deficits and oxidative stress injury in an amyloid β-peptide (25-35)-induced rodent model of Alzheimer's disease.
机构信息
Drug Clinical Trial Institution.
Department of Quality Management, The Third Affiliated Hospital of Zunyi Medical University, The First People's Hospital of Zunyi, Zunyi.
出版信息
Neuroreport. 2022 Jan 19;33(2):61-71. doi: 10.1097/WNR.0000000000001755.
OBJECTIVES
To verify whether mesenchymal stem cells cocultured with tanshinone IIA may ameliorate Alzheimer's disease by inhibiting oxidative stress.
METHODS
Sixty male Sprague-Dawley rats were randomly divided into 4 groups named Sham, Aβ25-35, mesenchymal stem cells, and mesenchymal stem cells (tanshinone IIA). The rats were treated according to different groups. The neurobehavioral performance of Sprague-Dawley rats was evaluated via Morris water maze test. Histological changes were checked via hematoxylin-eosin staining. The levels of total antioxidant activity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX) and malondialdehyde in hippocampus were assayed by ELISA kit. The levels of Aβ, p-tau/tau, and p-AMP-activated protein kinase/AMP-activated protein kinase in hippocampus were checked by Western blot.
RESULTS
Our research showed that the injection of mesenchymal stem cells (tanshinone IIA) into the hippocampus alleviated learning and memory deficits and reduced hippocampal neuronal injury in the Alzheimer's disease rats. Moreover, mesenchymal stem cells (tanshinone IIA) treatment suppressed oxidative stress, attenuated Aβ accumulation reduced Tau hyperphosphorylation, and enhanced the activity of AMP-activated protein kinase in the hippocampus of the Alzheimer's disease rats. However, there were almost no significant difference between the mesenchymal stem cells and Aβ25-35 groups.
CONCLUSIONS
Mesenchymal stem cells (tanshinone IIA) transplantation may be a potential treatment for curing Alzheimer's disease, which may be related to the inhibition of oxidative stress.
目的
验证丹参酮 IIA 共培养的间充质干细胞是否通过抑制氧化应激改善阿尔茨海默病。
方法
将 60 只雄性 Sprague-Dawley 大鼠随机分为 4 组，分别命名为 Sham、Aβ25-35、间充质干细胞和间充质干细胞（丹参酮 IIA）。根据不同的组进行治疗。通过 Morris 水迷宫试验评估 Sprague-Dawley 大鼠的神经行为表现。通过苏木精-伊红染色检查组织学变化。通过 ELISA 试剂盒测定海马组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-PX）和丙二醛（MDA）的总抗氧化活性（T-AOC）水平。通过 Western blot 检测海马组织中 Aβ、p-tau/tau 和 p-AMP 激活蛋白激酶/AMP 激活蛋白激酶的水平。
结果
我们的研究表明，向海马体注射间充质干细胞（丹参酮 IIA）可改善阿尔茨海默病大鼠的学习和记忆障碍，并减轻海马体神经元损伤。此外，间充质干细胞（丹参酮 IIA）治疗抑制了氧化应激，减轻了 Aβ 的积累，降低了 Tau 的过度磷酸化，增强了阿尔茨海默病大鼠海马体中 AMP 激活蛋白激酶的活性。然而，间充质干细胞和 Aβ25-35 组之间几乎没有明显差异。
结论
间充质干细胞（丹参酮 IIA）移植可能是治疗阿尔茨海默病的一种潜在方法，这可能与抑制氧化应激有关。
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