Effect of Bee Venom on an Experimental Cellular Model of Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disease and is characterized by the deposition of the β -Amyloid peptide (β A), which causes the inflammation of neurons. Bee venom (BV) elicits a strong anti-inflammatory response, and therefore we conducted an in vitro experiment to study the efficacy of BV in an AD cellular model. To mimic AD, the U87MG cell line was incubated for 168 hours with 2.5 μ M β A. Changes were confirmed by microscopy, and peptides were measured under stain-free conditions using homo-tomography. Sulforhodamine B analysis was performed to analyze the cell viability. Real-Time quantitative polymerase chain reaction (qPCR) analysis was conducted to analyze mRNA expression levels of pro-inflammatory cytokines (NF- κ B, COX-2, TNF- α , IL-1), and Western blot was performed to measure the Caspase-3 protein levels. BV showed no cytotoxicity at concentrations below 10 μ g/mL. The NF- κ B mRNA levels were not significantly different between the BV group and the control group. The amount of β A accumulation in the BV group decreased significantly. The mRNA expression levels of COX-2, TNF- α , and IL-1 were significantly reduced using 10 μ g/mL of BV compared to those in the control group. Additionally, Caspase-3 levels were also reduced compared to those of the control group when BV was used at a concentration of 10 μ g/mL. BV could inhibit apoptosis and inflammatory responses in an AD cellular model. In addition, it prevented cell accumulation of β A, an important pathogenic mechanism in AD. [ABSTRACT FROM AUTHOR]