PDF(Pubmed)
Abstract：
UNASSIGNED: Vascular cognitive impairment (VCI) is the second leading cause of dementia. Cognitive impairment is a common consequence of VCI. However, there is no effective treatment for VCI and the underlying mechanism of its pathogenesis remains unclear. This study to investigate whether artesunate (ART) can improve the learning and memory function in rats with VCI by down-regulating he level of autophagy in cerebral cortex neurons.
UNASSIGNED: The models for VCI were the rat bilateral common carotid artery occlusion (BACCO), which were randomized into three groups including the sham operation group (Sham), model + vehicle group (Model) and model + ART group (ART). Then the animal behaviors were recorded, as well as staining the results of cortical neurons. Western blot was performed to determine the protein expressions of LC3BⅡ/Ⅰ, p-AMPK, p-mTOR, and Beclin-1.
UNASSIGNED: Behavioral outcomes and the protein expressions in Model group were supposedly affected by the induction of autophagy in cerebral cortex neurons. Compared to the Model group, ART improved memory impairment in VCI rats. And the expression of LC3BⅡ/Ⅰ, p-AMPK/AMPK, Beclin-1 is significant decreased in the ART group, while significant increases of p-mTOR/mTOR were showed. These results suggest that ART improved learning and memory impairment in VCI rats by down-regulating the level of autophagy in cerebral cortex neurons.
UNASSIGNED: The results suggest that autophagy occurs in cerebral cortex neurons in rats with VCI. It is speculated that ART can improve learning and memory impairment in VCI rats by down-regulating the level of autophagy in cerebral cortex neurons.
UNASSIGNED: The models for VCI were the rat bilateral common carotid artery occlusion (BACCO), which were randomized into three groups including the sham operation group (Sham), model + vehicle group (Model) and model + ART group (ART). Then the animal behaviors were recorded, as well as staining the results of cortical neurons. Western blot was performed to determine the protein expressions of LC3BⅡ/Ⅰ, p-AMPK, p-mTOR, and Beclin-1.
UNASSIGNED: Behavioral outcomes and the protein expressions in Model group were supposedly affected by the induction of autophagy in cerebral cortex neurons. Compared to the Model group, ART improved memory impairment in VCI rats. And the expression of LC3BⅡ/Ⅰ, p-AMPK/AMPK, Beclin-1 is significant decreased in the ART group, while significant increases of p-mTOR/mTOR were showed. These results suggest that ART improved learning and memory impairment in VCI rats by down-regulating the level of autophagy in cerebral cortex neurons.
UNASSIGNED: The results suggest that autophagy occurs in cerebral cortex neurons in rats with VCI. It is speculated that ART can improve learning and memory impairment in VCI rats by down-regulating the level of autophagy in cerebral cortex neurons.
摘要：
■血管性认知障碍（VCI）是痴呆的第二大原因。认知障碍是VCI的常见后果。然而,目前尚无有效的VCI治疗方法,其发病机制尚不清楚.本研究旨在探讨青蒿琥酯(ART)能否通过下调大脑皮质神经元自噬水平来改善VCI大鼠的学习记忆功能。
■VCI模型为大鼠双侧颈总动脉闭塞（BACCO），随机分为三组，包括假手术组（Sham），模型+车辆组(模型)和模型+ART组(ART)。然后记录动物的行为，以及染色皮质神经元的结果。Westernblot检测LC3BⅡ/Ⅰ蛋白的表达,p-AMPK,p-mTOR,还有Beclin-1.
■模型组的行为结果和蛋白表达可能受到大脑皮层神经元自噬诱导的影响。与“模型”组相比，ART改善了VCI大鼠的记忆障碍。LC3BⅡ/Ⅰ的表达,p-AMPK/AMPK,Beclin-1在ART组中显著降低，而p-mTOR/mTOR显著增加。这些结果表明，ART通过下调大脑皮层神经元自噬水平来改善VCI大鼠的学习和记忆障碍。
■结果表明，VCI大鼠大脑皮层神经元存在自噬。推测ART可通过下调大脑皮质神经元自噬水平改善VCI大鼠学习记忆障碍。
■VCI模型为大鼠双侧颈总动脉闭塞（BACCO），随机分为三组，包括假手术组（Sham），模型+车辆组(模型)和模型+ART组(ART)。然后记录动物的行为，以及染色皮质神经元的结果。Westernblot检测LC3BⅡ/Ⅰ蛋白的表达,p-AMPK,p-mTOR,还有Beclin-1.
■模型组的行为结果和蛋白表达可能受到大脑皮层神经元自噬诱导的影响。与“模型”组相比，ART改善了VCI大鼠的记忆障碍。LC3BⅡ/Ⅰ的表达,p-AMPK/AMPK,Beclin-1在ART组中显著降低，而p-mTOR/mTOR显著增加。这些结果表明，ART通过下调大脑皮层神经元自噬水平来改善VCI大鼠的学习和记忆障碍。
■结果表明，VCI大鼠大脑皮层神经元存在自噬。推测ART可通过下调大脑皮质神经元自噬水平改善VCI大鼠学习记忆障碍。
