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Jin-Lan Huang [1; 2] and Ying-Qin Feng [3] and Li-Ru Bai [2] and Mei-Chun Qin [4] and Zhe-Hao Xu [4] and Zhao-Rong Liu [2] and Wen-Bing Chen [2] and Deng-Pan Wu [1; 2] and Zhen-Guo Zhong [4]

Academic Editor: Krishnadas Nandakumar

1, Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Pharmacy School, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China, xzmc.edu.cn

2, Department of Pharmacology, Pharmacy School, Xuzhou Medical University, Xuzhou, Jiangsu 221004, China, xzmc.edu.cn

3, Department of Pharmacy, Liuzhou Traditional Chinese Medical Hospital, Liuzhou, Guangxi 545001, China, liuzhou.gov.cn

4, Scientific Research Center of Traditional Chinese Medicine, Guangxi University of Chinese Medicine, Nanning, Guangxi 530200, China, gxtcm.com

Received Jun 1, 2017; Revised Aug 14, 2017; Accepted Aug 23, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Alzheimer’s disease (AD), the most prevalent cause of dementia worldwide, is defined neuropathologically by the deposition of amyloid-β peptides (Aβ) into senile plaques in the extracellular space, neuronal cell death induced by oxidative stress, and intracellular formation of neurofibrillary tangles. The senile plaque is mainly composed of Aβ with length of 40 or 42 residues. Aβ is generated from β-amyloid precursor protein (APP) firstly cleaved by β-secretase (β-APP cleaving enzyme 1, BACE1) and then by γ-secretase. Abnormal accumulation of extracellular Aβ in amyloid plaques causes neuronal damage, impairment of cognitive function, and ultimately the development of dementia [1]. Furthermore, growing evidence suggests that oxidative stress plays important roles in Aβ deposition and cognitive dysfunction of AD. It has been established that Aβ induces oxidative stress and oxidative stress in turn enhances the Aβ production and aggregation, which promotes neuronal degeneration and death, resulting in cognitive function impairment [2]. Antioxidant treatments in the early stage of AD pathogenesis were able to alleviate the cognitive function impairment and reduce Aβ accumulation in AD [3]. Accordingly, identification of potential protective candidates to attenuate oxidative stress and eliminate excessive accumulation of Aβ and ultimately improve cognitive function impairment is considered as an important strategy for AD treatment.

Radix Notoginseng, a widely...

  

  

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