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Article Publish Status: FREE
Abstract Title:

Ginsenoside compound K attenuates cognitive deficits in vascular dementia rats by reducing the Aβ deposition.

Abstract Source:

J Pharmacol Sci. 2019 Mar ;139(3):223-230. Epub 2019 Feb 13. PMID: 30799178

Abstract Author(s):

Wenjing Zong, Xiangchang Zeng, Siyu Chen, Lulu Chen, Luping Zhou, Xintong Wang, Qing Gao, Guirong Zeng, Kai Hu, Dongsheng Ouyang

Article Affiliation:

Wenjing Zong

Abstract:

Ginsenoside compound K (CK) is the main metabolite of protopanaxadiol-type ginsenosides and has been demonstrated to exert neuroprotective and cognition-enhancing effects. The effects of CK on cognitive function in vascular dementia (VD) has not been elucidated. Therefore, the present study aims to elucidate the effects of CK on memory function as well as its potential mechanism in VD rats. Sprague-Dawley rats were subjected to Chronic Cerebral Hypoperfusion (CCH) by permanent bilateral common carotid artery occlusion (2VO). CCH induced neuronal damage and aggravated the aggregation of Amyloid-βpeptides (Aβ), which plays a critical role in the neurotoxicity and cognitive impairment. CK treatment attenuated CCH-induced Aβdeposition and ameliorated cognition impairment. Furthermore, CK enhanced the activity of the pSer9-Glycogen synthase kinase 3β (pSer9-GSK3β) and the insulin degrading enzyme (IDE), which mainly involved the production and clearance of Aβ. Moreover, CK treatment enhanced the activity of protein kinase B (PKB/Akt), a key kinase in phosphatidylinositol 3 kinase (PI3K)/Akt pathway that can regulate the activity of GSK-3β and IDE. In short, our findings provide the first evidence that CK might attenuate cognitive deficits and Aβdeposition in the hippocampus via enhancing the expression of pSer9-GSK-3β and IDE.

Study Type : Animal Study

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