Department of Acupuncture & Moxibustion Medicine, College of Korean Medicine Daejeon University, 62, Daehak-ro, Dong-gu, Daejeon, Republic of Korea.
Department of Acupuncture & Moxibustion Medicine, Cheonan Korean Medicine Hospital of Daejeon University, 4, Notaesan-ro, Seobuk-gu, Cheonan-si Chungcheongnam-do, Republic of Korea.
Am J Chin Med. 2020;48(8):1803-1819. doi: 10.1142/S0192415X20500901. Epub 2020 Dec 9.
Alzheimer's disease (AD) is a neurodegenerative disease and is characterized by the deposition of the [Formula: see text]-Amyloid peptide ([Formula: see text]A), which causes the inflammation of neurons. Bee venom (BV) elicits a strong anti-inflammatory response, and therefore we conducted an 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 [Formula: see text]M [Formula: see text]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-[Formula: see text]B, COX-2, TNF-[Formula: see text], IL-1), and Western blot was performed to measure the Caspase-3 protein levels. BV showed no cytotoxicity at concentrations below 10 [Formula: see text]g/mL. The NF-[Formula: see text]B mRNA levels were not significantly different between the BV group and the control group. The amount of [Formula: see text]A accumulation in the BV group decreased significantly. The mRNA expression levels of COX-2, TNF-[Formula: see text], and IL-1 were significantly reduced using 10 [Formula: see text]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 [Formula: see text]g/mL. BV could inhibit apoptosis and inflammatory responses in an AD cellular model. In addition, it prevented cell accumulation of [Formula: see text]A, an important pathogenic mechanism in AD.
阿尔茨海默病（AD）是一种神经退行性疾病，其特征是[公式：见文本]-淀粉样肽（[公式：见文本]A）的沉积，导致神经元炎症。蜂毒（BV）引起强烈的抗炎反应，因此我们进行了一项实验，以研究 BV 在 AD 细胞模型中的疗效。为了模拟 AD，将 U87MG 细胞系用 2.5 [公式：见文本]M [公式：见文本]A 孵育 168 小时。通过显微镜观察确认变化，并在无染色条件下使用同型断层摄影术测量肽。使用 Sulforhodamine B 分析来分析细胞活力。进行实时定量聚合酶链反应（qPCR）分析以分析促炎细胞因子（NF-[公式：见文本]B、COX-2、TNF-[公式：见文本]、IL-1）的 mRNA 表达水平，并进行 Western blot 以测量 Caspase-3 蛋白水平。BV 在低于 10 [公式：见文本]g/mL 的浓度下没有细胞毒性。BV 组和对照组之间的 NF-[公式：见文本]B mRNA 水平没有显着差异。BV 组[公式：见文本]A 积累量显着减少。与对照组相比，用 10 [公式：见文本]g/mL 的 BV 处理后，COX-2、TNF-[公式：见文本]和 IL-1 的 mRNA 表达水平显着降低。此外，与对照组相比，当使用 10 [公式：见文本]g/mL 的 BV 时，Caspase-3 水平也降低。BV 可以抑制 AD 细胞模型中的细胞凋亡和炎症反应。此外，它可以防止 AD 中重要的致病机制[公式：见文本]A 的细胞积累。
