Steamed and Fermented Ethanolic Extract from Codonopsis lanceolata Attenuates Amyloid-β-Induced Memory Impairment in Mice.

Jin Bae Weon,Choong Je Ma,Eun-Hye Hong,Dong-Sik Park,Hyeon Yong Lee,Min Rye Eom,Hyun-Jeong Ko,Youn Sik Jung

doi:10.1155/2016/1473801

Abstract

Codonopsis lanceolata (C. lanceolata) is a traditional medicinal plant used for the treatment of certain inflammatory diseases such as asthma, tonsillitis, and pharyngitis. We evaluated whether steamed and fermented C. lanceolata (SFC) extract improves amyloid-β- (Aβ-) induced learning and memory impairment in mice. The Morris water maze and passive avoidance tests were used to evaluate the effect of SFC extract. Moreover, we investigated acetylcholinesterase (AChE) activity and brain-derived neurotrophic factor (BDNF), cyclic AMP response element-binding protein (CREB), and extracellular signal-regulated kinase (ERK) signaling in the hippocampus of mice to determine a possible mechanism for the cognitive-enhancing effect. Saponin compounds in SFC were identified by Ultra Performance Liquid Chromatography-Quadrupole-Time-of-Flight Mass Spectrometry (UPLC-Q-TOF-MS). SFC extract ameliorated amyloid-β-induced memory impairment in the Morris water maze and passive avoidance tests. SFC extract inhibited AChE activity and also significantly increased the level of CREB phosphorylation, BDNF expression, and ERK activation in hippocampal tissue of amyloid-β-treated mice. Lancemasides A, B, C, D, E, and G and foetidissimoside A compounds present in SFC were determined by UPLC-Q-TOF-MS. These results indicate that SFC extract improves Aβ-induced memory deficits and that AChE inhibition and CREB/BDNF/ERK expression is important for the effect of the SFC extract. In addition, lancemaside A specifically may be responsible for efficacious effect of SFC.

Highlights

Alzheimer’s disease (AD) is the most common progressive neurodegenerative disorder, causing memory and cognition impairment [1]
The untreated memory impaired group, showed a shorter time spent in the target quadrant than the control group, and the swimming time in the target quadrant by the untreated memory impaired mice was significantly increased when treated with steamed and fermented C. lanceolata (SFC) (p < 0.005) (Figure 3)
We evaluated the effect of SFC on Aβinduced memory impairment in mice using the Morris water maze and passive avoidance tests

Summary

Introduction

Alzheimer’s disease (AD) is the most common progressive neurodegenerative disorder, causing memory and cognition impairment [1]. There are multiple causes of AD and it is likely that some causes have yet to be discovered. The characteristic pathogenesis of AD is accumulation of amyloid-β(Aβ-) containing senile plaques and neurofibrillary tangles in the brain that lead to inflammation in surrounding tissue [2]. The presence of neurofibrillary tangles, composed of hyperphosphorylated tau (a microtubule-associated protein), and senile plaques correlate with cellular dysfunction. Aβ plays a significant role in the development of AD [3,4,5]. Acetylcholine (ACh) is a neurotransmitter involved in memory and learning processing in the cholinergic system. High AChE activity is present in the brains of AD patients [6, 7]

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Conclusion