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首页> 外文期刊>Evidence-based complementary and alternative medicine: eCAM >The Effects of Yuan-Zhi Decoction and Its Active Ingredients in Both In Vivo and In Vitro Models of Chronic Cerebral Hypoperfusion by Regulating the Levels of Aβ and Autophagy
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The Effects of Yuan-Zhi Decoction and Its Active Ingredients in Both In Vivo and In Vitro Models of Chronic Cerebral Hypoperfusion by Regulating the Levels of Aβ and Autophagy

机译：通过调节Aβ和自噬调节慢性脑低渗慢性脑低渗的体内和体外模型中的袁智汤及其活性成分的影响

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Chronic cerebral hypoperfusion (CCH) is closely related to the occurrence of Alzheimer’s disease (AD) in the elderly. CCH can induce overactivation of autophagy, which increases the deposition of amyloid-β (Aβ) plaques in the brain, eventually impairing the cognitive function. Yuan-Zhi decoction (YZD) is a traditional Chinese medicine (TCM) formulation that is used to treat cognitive dysfunction in the elderly, but the specific mechanism is still unclear. In this study, we simulated CCH in a rat model through bilateral common carotid artery occlusion (BCCAO) and treated the animals with YZD. Standard neurological tests indicated that YZD significantly restored the impaired cognitive function after BCCAO in a dose-dependent manner. Furthermore, YZD also decreased the levels of Aβ aggregates and the autophagy-related proteins ATG5 and ATG12 in their hippocampus. An in vitro model of CCH was also established by exposing primary rat hippocampal neurons to hypoxia and hypoglycemia (H-H). YZD and its active ingredients increased the survival of these neurons and decreased the levels of Aβ1-40 and Aβ1-42, autophagy-related proteins Beclin-1 and LC3-II, and the APP secretases BACE1 and PS-1. Finally, both Aβ aggregates showed a positive statistical correlation with the expression levels of the above proteins. Taken together, YZD targets Aβ, autophagy, and APP-related secretases to protect the neurons from hypoxic-ischemic injury and restore cognitive function.
机译：慢性脑低渗（CCH）与老年人的阿尔茨海默病（AD）发生密切相关。 CCH可以诱导自噬的过度激活，这增加了大脑中淀粉样蛋白-β（Aβ）斑块的沉积，最终损害认知功能。袁智汤（YZD）是一种中药（TCM）制剂，用于治疗老年人的认知功能障碍，但具体机制尚不清楚。在这项研究中，我们通过双侧常见的颈动脉闭塞（BCCAO）来模拟大鼠模型中的CCH，并用YZD处理动物。标准神经系统试验表明，YZD以剂量依赖性方式显着恢复了BCCAO后的认知功能受损。此外，YZD还降低了其海马中Aβ聚集体和自噬相关蛋白ATG5和ATG12的水平。还通过将原发性大鼠海马神经元暴露于缺氧和低血糖血症（H-H）来建立CCH体外模型。 YZD及其活性成分增加了这些神经元的存活率，并降低了Aβ1-40和Aβ1-42，自噬相关蛋白质BEC1和LC3-II的水平，以及APP分泌​​酶Bace1和PS-1。最后，两个Aβ聚集体显示出与上述蛋白质的表达水平的阳性统计相关性。 yzd占Aβ，自噬和应用相关分泌酶，以保护神经元免受缺氧缺血性损伤和恢复认知功能。

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