Abstract
Royal jelly (RJ), a hive product with versatile pharmacological activities, has been used as a traditional functional food to prevent or treat inflammatory diseases. However, little is known about the anti-inflammatory effect of RJ in microglial cells. The aim of this study is to assess the anti-inflammatory effects of RJ in lipopolysaccharide- (LPS-) induced murine immortalized BV-2 cells and to explore the underlying molecular mechanisms. Our results showed that in LPS-stimulated BV-2 cells, RJ significantly inhibited iNOS and COX-2 expression at mRNA and protein levels. The mRNA expression of IL-6, IL-1β, and TNF-α was also downregulated by RJ in a concentration-dependent manner. Additionally, RJ protected BV-2 cells against oxidative stress by upregulating heme oxygenase-1 (HO-1) expression and by reducing reactive oxygen species (ROS) and nitric oxide (NO) production. Mechanistically, we found that RJ could alleviate inflammatory response in microglia by suppressing the phosphorylation of IκBα, p38, and JNK and by inhibiting the nucleus translocation of NF-κB p65. These findings suggest that RJ might be a promising functional food to delay inflammatory progress by influencing the microglia function.
Highlights
It is noteworthy that inflammation in the central nervous system (CNS) is associated with the occurrence and progression of some neurodegenerative diseases, including Alzheimer’s disease (AD) [1]
To determine the appropriate concentrations of Royal jelly (RJ) treatments, we carried out the cell counting kit-8 assay to measure the viability of cells treated by RJ alone and cells cotreated with RJ/LPS (Figure 1)
Based on our cell viability histogram, treatments of RJ up to 3 mg/mL for 24 h had no cytotoxic effects in comparison with the control group
Summary
It is noteworthy that inflammation in the central nervous system (CNS) is associated with the occurrence and progression of some neurodegenerative diseases, including Alzheimer’s disease (AD) [1]. At the end of the 1980s, McGeer and Rogers reported that there were lots of activated glia cells in the AD brain [3, 4]. An elevated level of interleukin-18 (IL-18), a detrimental inflammatory cytokine, has been reported in the brains of AD patients [5]. Microglia will switch to an activated phenotype (M1 type) and generate highly detrimental mediators when their microenvironment becomes stressful. All of these neurotoxic mediators will do harm to neurons and glial cells, and the brain homeostasis will be disturbed, which is the main cause of most neurodegenerative diseases [10]. It was reported that lipopolysaccharide (LPS), a bacterial endotoxin, could stimulate
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