Abstract

In the previous work, we found PRG, a polysaccharide from Phellinus ribis, exhibited neurotrophic activity. To obtain an active structural unit with lower molecular weight, PRG was degraded to prepare the degraded PRG (DPRG) using ascorbic acid and H2O2. The aim of the paper was to obtain DPRG by optimizing the degradation conditions using response surface methodology (RSM) and to study its protective effects of PC12 cells induced by Aβ25–35. The optimum conditions were as follows; the concentration of H2O2-Vc was 17 mM and degradation temperature was 50 °C; when degradation time was 1.6 h, the experimental response value of PC12 cell viability was 83.4 ± 0.15%, which was in accordance with the predicted value (83.5%). We also studied the protective effects of DPRG against the Aβ25–35-induced neurotoxicity and explored the underlying mechanism. The results showed that treatment with DPRG could attenuate PC12 cells death. The mechanism was relative to the inhibition of cell apoptosis by increasing the MMP level and decreasing the protein expression of cytochrome C (Cytc) in PC12 cells. In conclusion, DPRG with lower molecular weight was obtained successfully. It possessed neuroprotective properties and might be a candidate for neurodegenerative disease treatment.

Highlights

  • Alzheimer’s disease (AD) is a deadly chronic neurodegenerative disorder in the world, which contributes to memory loss and cognitive decline in the elderly [1,2]

  • This paper demonstrates the of PC12 cells was associated with mitochondrial membrane potential and inhibition of degraded PRG (DPRG) on the apoptosis of PC12 cells was associated with

  • More and more evidence indicates that natural polysaccharides extracted from animals plants possess rangeand of biological activities, for example, At present, there is no effectiveand treatment for AD.aMore more evidence indicates that theynatural exhibitpolysaccharides antioxidant properties

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Summary

Introduction

Alzheimer’s disease (AD) is a deadly chronic neurodegenerative disorder in the world, which contributes to memory loss and cognitive decline in the elderly [1,2]. Aβ25–35 , the toxic peptide fragment of the full-length Aβ peptide, could induce a direct toxic effect on the neurons, leading to apoptosis of neurons [5,6]. As it has been recently shown, the toxicity of peptide fragments, such as. In the present paper, the inhibition of Aβ-induced neuronal apoptosis may provide a promising approach for the prevention and treatment of neurodegenerative diseases especially AD

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