Abstract
Alzheimer’s disease (AD) is the most common form of dementia characterized by aggregation of amyloid β (Aβ) and neuronal loss. One of the risk factors for AD is high cholesterol levels, which are known to promote Aβ deposition. Previous studies have shown that royal jelly (RJ), a product of worker bees, has potential neuroprotective effects and can attenuate Aβ toxicity. However, little is known about how RJ regulates Aβ formation and its effects on cholesterol levels and neuronal metabolic activities. Here, we investigated whether RJ can reduce cholesterol levels, regulate Aβ levels and enhance neuronal metabolic activities in an AD rabbit model induced by 2% cholesterol diet plus copper drinking water. Our results suggest that RJ significantly reduced the levels of plasma total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C), and decreased the level of Aβ in rabbit brains. RJ was also shown to markedly ameliorate amyloid deposition in AD rabbits from Aβ immunohistochemistry and thioflavin-T staining. Furthermore, our study suggests that RJ can reduce the expression levels of β-site APP cleaving enzyme-1 (BACE1) and receptor for advanced glycation end products (RAGE), and increase the expression levels of low density lipoprotein receptor-related protein 1 (LRP-1) and insulin degrading enzyme (IDE). In addition, we found that RJ remarkably increased the number of neurons, enhanced antioxidant capacities, inhibited activated-capase-3 protein expression, and enhanced neuronal metabolic activities by increasing N-acetyl aspartate (NAA) and glutamate and by reducing choline and myo-inositol in AD rabbits. Taken together, our data demonstrated that RJ could reduce cholesterol levels, regulate Aβ levels and enhance neuronal metabolic activities in AD rabbits, providing preclinical evidence that RJ treatment has the potential to protect neurons and prevent AD.
Highlights
Alzheimer’s disease (AD), the most common type of dementia, is a primary degenerative disease that occurs in the central nervous system (CNS)
Compared with the AD model group, plasma total cholesterol (TC) and low density lipoprotein-cholesterol (LDL-C) levels in the royal jelly (RJ) group were significantly reduced by 28% and 23% respectively, while there was no significant difference in plasma High-Density Lipoprotein Cholesterol (HDL-C) levels between the RJ group and the AD model group (p = 0.07)
Our study confirmed in a rabbit AD model that hypercholesterolemia promotes amyloid β (Aβ) deposition and leads to neuronal loss, whereas RJ has the effects of reducing plasma TC and LDL-C levels, enhancing anti-oxidative capacities, FIGURE 7 | RJ improved brain metabolic activities in AD rabbits. (A) Regions of interest (ROI) location in the brain and representative spectra from the AD model, RJ and normal control (NC) group rabbits
Summary
Alzheimer’s disease (AD), the most common type of dementia, is a primary degenerative disease that occurs in the central nervous system (CNS). It was recently reported that RJ significantly improves spatial learning and memory in rats with streptozotocin-induced SAD (Zamani et al, 2012), and that RJ attenuates Aβ toxicity in a C. elegans model of AD (Wang et al, 2016). Despite these latest research developments in RJ’s potential treatment effects related to AD, the mechanism of how RJ regulates Aβ formation and delays the development of AD remains elusive
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