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. 2017 Feb 4;9(2):105.
doi: 10.3390/nu9020105.

Lychee Seed Saponins Improve Cognitive Function and Prevent Neuronal Injury via Inhibiting Neuronal Apoptosis in a Rat Model of Alzheimer's Disease

Xiuling Wang  1 , Jianming Wu  2 , Chonglin Yu  3 , Yong Tang  4 , Jian Liu  5 , Haixia Chen  6 , Bingjin Jin  7 , Qibing Mei  8 , Shousong Cao  9 , Dalian Qin  10
Affiliations

Lychee Seed Saponins Improve Cognitive Function and Prevent Neuronal Injury via Inhibiting Neuronal Apoptosis in a Rat Model of Alzheimer's Disease

Xiuling Wang et al. Nutrients. .

Abstract

Lychee seed is a traditional Chinese medicine and possesses many activities, including hypoglycemia, liver protection, antioxidation, antivirus, and antitumor. However, its effect on neuroprotection is still unclear. The present study investigated the effects of lychee seed saponins (LSS) on neuroprotection and associated mechanisms. We established a rat model of Alzheimer's disease (AD) by injecting Aβ25-35 into the lateral ventricle of rats and evaluated the effect of LSS on spatial learning and memory ability via the Morris water maze. Neuronal apoptosis was analyzed by hematoxylin and eosin stain and terminal deoxynucleotidyl transferase (Tdt)-mediated dUTP nick-end labeling analysis, and mRNA expression of caspase-3 and protein expressions of Bax and Bcl-2 by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. The results showed that LSS remarkably improved cognitive function and alleviated neuronal injury by inhibiting apoptosis in the hippocampus of AD rats. Furthermore, the mRNA expression of caspase-3 and the protein expression of Bax were downregulated, while the protein expression of Bcl-2 and the ratio of Bcl-2/Bax were increased by LSS. We demonstrate that LSS significantly improves cognitive function and prevent neuronal injury in the AD rats via regulation of the apoptosis pathway. Therefore, LSS may be developed as a nutritional supplement and sold as a drug for AD prevention and/or treatment.

Keywords: Alzheimer’s disease; apoptosis; cognitive function; lychee seed saponins; neuronal injury; rat model of Alzheimer’s disease.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
The chemical profile of LSS determined by a UHPLC-SPD chromatogram.
Figure 2
Figure 2
Effects of LSS and donepezil (Don) on the ability of spatial learning and memory in rats. (A). Escape latency: ● control rats treated with NS; ■ AD rats treated with NS; ▲ donepezil 0.42 mg/kg; ▼ LSS 120 mg/kg; ♦ LSS 240 mg/kg; formula image LSS 480 mg/kg; (B) Number of times across the platform; (C) platform quadrant dwell time; and (D) percentage of the total distance run in the platform quadrant. There were 10 rats used for each experimental group and expressed as the mean ± SD. ** p < 0.01 vs. the AD rats treated with NS (control).
Figure 3
Figure 3
Protective effects of LSS and donepezil on neurons injury induced by Aβ25–35 in the hippocampus of AD rats (400×). (A) Histologic picture of neurons in the control rat treated with NS, shows preserved normal histological features of neurons; (B) Histologic picture of neurons in the AD rat treated with NS, shows damaged neurons; (C) Histologic picture of neurons in the AD rat treated with donepezil 0.42 mg/kg, shows near normal histological features of neurons; (D) Histologic picture of neurons in the AD rat treated with LSS 120 mg/kg, shows near normal histological features of neurons; (E) Histologic picture of neurons in the AD rat treated with LSS 240 mg/kg, shows near normal histological features of neurons; (F) Histologic picture of neurons in the AD rat treated with LSS 480 mg/kg, shows normal histological features of neurons. Each group had three rats.
Figure 4
Figure 4
Effects of LSS and donepezil on neuronal apoptosis induced by Aβ25–35 in the hippocampus of control (normal) and AD rats (400×). (A) Neuronal cells in the control rat treated with NS; (B) Neuronal cells in the AD rat treated with NS; (C) Neuronal cells in the AD rat treated with donepezil 0.42 mg/kg; (D) Neuronal cells in the AD rat treated with LSS 120 mg/kg; (E) Neuronal cells in the AD rat treated with LSS 240 mg/kg; (F) Neuronal cells in the AD rat treated with LSS 480 mg/kg. The results are representative of at least three independent experiments.
Figure 5
Figure 5
Percentages of apoptosis in the sections of the neuronal cells in the hippocampus of rats. The results are representative of at least three independent experiments and expressed as the mean ± SD. ** p < 0.01 vs. the AD rats treated with NS (control).
Figure 6
Figure 6
Effects of LSS and donepezil (Don) on the mRNA expressions of caspase-3 in the brain tissues of rats (A) The bands of caspase-3 mRNA and β-actin; (B) The ratio of caspase-3 mRNA and β-actin. The results are representative of at least three independent experiments and expressed as the mean ± SD. ** p < 0.01 vs. the AD rats treated with NS (control).
Figure 7
Figure 7
Effect of LSS on the protein expressions of Bax and Bcl-2 in PC12 cells. (A) The bands of Bax, Bcl-2 protein and β-actin; (B) The ratio of Bax protein and β-actin; (C) The ratio of Bcl-2 protein and β-actin; (D) The ratio of Bcl-2 protein and Bax. The results are representative of at least three independent experiments run in triplicate and expressed as the mean ± SD. ** p < 0.01, vs. the cells treated with Aβ25–35 and medium (vehicle control).
Figure 8
Figure 8
LSS improves cognitive function and prevents neuronal injury of AD rats via inhibiting the neuronal apoptosis signaling pathway.
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