Phytoceramide shows neuroprotection and ameliorates scopolamine-induced memory impairment.

Jae-Chul Jung,Jong Hoon Ryu,Yeonju Lee,Sohyeon Moon,Seikwan Oh

doi:10.3390/molecules16119090

Jae-Chul Jung, Jong Hoon Ryu + Show 3 more

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https://doi.org/10.3390/molecules16119090

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Abstract

The function and the role phytoceramide (PCER) and phytosphingosine (PSO) in the central nervous system has not been well studied. This study was aimed at investigating the possible roles of PCER and PSO in glutamate-induced neurotoxicity in cultured neuronal cells and memory function in mice. Phytoceramide showed neuro-protective activity in the glutamate-induced toxicity in cultured cortical neuronal cells. Neither phytosphingosine nor tetraacetylphytosphingosine (TAPS) showed neuroproective effects in neuronal cells. PCER (50 mg/kg, p.o.) recovered the scopolamine-induced reduction in step-through latency in the passive avoidance test; however, PSO did not modulate memory function on this task. The ameliorating effects of PCER on spatial memory were confirmed by the Morris water maze test. In conclusion, through behavioral and neurochemical experimental results, it was demonstrated that central administration of PCER produces amelioration of memory impairment. These results suggest that PCER plays an important role in neuroprotection and memory enhancement and PCER could be a potential new therapeutic agent for the treatment of neurodegenerative diseases such as Alzheimer’s disease.

Highlights

The major pathogenic mechanisms of neuronal damage include excitotoxicity, production of reactive free radicals, inflammation, and programmed cell death [1]
Compounds were added to the culture medium with glutamate, and neuroprotection was observed via microscopic images and measuring the glutamate-induced Lactate dehydrogenases (LDH) release
In the present study it was observed that phytoceramide (PCER) showed neuroprotective effects in cultured neuronal cells and improves the memory impairment induced by scopolamine

Summary

Introduction

The major pathogenic mechanisms of neuronal damage include excitotoxicity, production of reactive free radicals, inflammation, and programmed cell death (apoptosis) [1]. Activation of glutamate receptors, through the attendant failure of ion homeostasis and increase in intracellular Ca2+. Concentration, is a major factor involved in initiating ischemic cell death [2]. A straightforward therapeutic approach, is to block the receptors that are activated by glutamate. It has been known that brain cholinergic system losses are closely associated with the cognitive deficits observed in Alzheimer’s disease [3]. An agent that can ameliorate cognitive dysfunction and neurotoxocity induced by glutamate or cholinergic dysfunction should be effective in the treatment of various neurodegenerative diseases, including Alzheimer’s disease. The scopolamineinduced amnesic animal model has been used to screen for potential treatments for cognitive dysfunction [5]

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