Comparative Neuroprotective Effects of Dietary Curcumin and Solid Lipid Curcumin Particles in Cultured Mouse Neuroblastoma Cells after Exposure to Aβ42.

Panchanan Maiti,Gary L Dunbar

doi:10.1155/2017/4164872

Abstract

Aggregation of amyloid beta protein (Aβ) and phosphorylated tau (p-Tau) plays critical roles in pathogenesis of Alzheimer's disease (AD). As an antiamyloid natural polyphenol, curcumin (Cur) has a potential role in prevention of neurodegeneration in AD. However, due to limited absorption of the dietary Cur, the solid lipid Cur particles (SLCP) have been suggested as being more effective for AD therapy. In the present study, we compared the role of dietary Cur and SLCP on oxidative stress, neuronal death, p-Tau level, and certain cell survival markers in vitro, after exposure to Aβ42. Mouse neuroblastoma cells were exposed to Aβ42 for 24 h and incubated with or without dietary Cur and/or SLCP. Reactive oxygen species (ROS), apoptotic cell death, p-Tau, and tau kinase (including GSK-3β and cell survival markers, such as total Akt, phosphorylated Akt, and PSD95 levels) were investigated. SLCP showed greater permeability than dietary Cur in vitro, decreased ROS production, and prevented apoptotic death. In addition, SLCP also inhibited p-Tau formation and significantly decreased GSK-3β levels. Further, the cell survival markers, such as total Akt, p-Akt, and PSD95 levels, were more effectively maintained by SLCP than dietary Cur in Aβ42 exposed cells. Therefore, SLCP may provide greater neuroprotection than dietary Cur in Alzheimer's disease.

Highlights

Alzheimer’s disease (AD) is an age-related, progressive neurological disorder characterized by memory impairment and neuropsychological disturbances [1, 2]
Our results suggest that solid lipid Cur particles (SLCP) has greater neuroprotective effects compared to dietary Cur in terms of restoring several cell survival proteins and decreasing neuronal death, in vitro, after exposure to Aβ2
We found greater cellular permeability in the case of SLCP after 2 and 4 h of incubation, when compared to dietary Cur (Figure 1(b))

Summary

Introduction

Alzheimer’s disease (AD) is an age-related, progressive neurological disorder characterized by memory impairment and neuropsychological disturbances [1, 2]. Neuroinflammation, oxidative stress, and failure in protein degradation pathways are associated with this complex disorder [1, 5, 6]. These processes decrease trophic support of neurons and contribute to the decline of cell survival mechanisms [7]. The maintenance of cell survival proteins markers as well as decreasing in oxidative stress is critical factor for preventing or delaying neurodegeneration or neuronal loss. Several attempts have been made to salvage degenerating neurons by using small molecules, drugs, and natural polyphenols, none of them have been able to prevent the loss of degenerating neurons in a significant manner. Some of the drugs have been used for symptombased treatments, such as acetylcholine esterase inhibitors (e.g., tacrine, physostigmine, and velnacrine) [9] or glutamate receptor inhibitors (e.g., memantine) [10] and can provide temporary symptomatic relief, and some of them are partially effective in restoring normal cognition and reducing neurobehavioral abnormalities, but they often produce adverse

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