Lin Ni-Hsuan, Goh Angela, Lin Shyh-Horng, Chuang Kai-An, Chang Chih-Hsuan, Li Ming-Han, Lu Chu-Hsun, Chen Wen-Yin, Wei Pei-Hsuan, Pan I-Hong, Perng Ming-Der, Wen Shu-Fang
Institute of Molecular Medicine, College of Life Sciences, National Tsing Hua University, Hsinchu, Taiwan.
Biomedical Technology and Device Research Laboratories, Industrial Technology Research Institute, Hsinchu, Taiwan.
J Alzheimers Dis Rep. 2023 Jan 27;7(1):51-76. doi: 10.3233/ADR-220056. eCollection 2023.
Alzheimer's disease (AD) is a multifactorial disorder characterized by cognitive decline. Current available therapeutics for AD have limited clinical benefit. Therefore, preventive therapies for interrupting the development of AD are critically needed. Molecules targeting multifunction to interact with various pathlogical components have been considered to improve the therapeutic efficiency of AD. In particular, herbal medicines with multiplicity of actions produce cognitive benefits on AD. Bugu-M is a multi-herbal extract composed of (Antler form), Gaertn., Mill., and with the ability of its various components to confer resilience to cognitive deficits.
To evaluate the potential of Bugu-M on amyloid-β (Aβ) toxicity and its mechanisms and on cognitive function.
We illustrated the effect of Bugu-M on Aβ-evoked toxicity as well as its possible mechanisms to diminish the pathogenesis of AD in rat cortical neurons. For cognitive function studies, 2-month-old female 3×Tg-AD mice were administered 400 mg/kg Bugu-M for 30 days. Behavioral tests were performed to assess the efficacy of Bugu-M on cognitive impairment.
In primary cortical neuronal cultures, Bugu-M mitigated Aβ-evoked toxicity by reducing cytoskeletal aberrations and axonal disruption, restoring presynaptic and postsynaptic protein expression, suppressing mitochondrial damage and apoptotic signaling, and reserving neurogenic and neurotrophic factors. Importantly, 30-day administration of Bugu-M effectively prevented development of cognitive impairment in 3-month-old female 3×Tg-AD mice.
Bugu-M might be beneficial in delaying the progression of AD, and thus warrants consideration for its preventive potential for AD.
阿尔茨海默病（AD）是一种以认知功能衰退为特征的多因素疾病。目前可用的AD治疗方法临床疗效有限。因此，迫切需要能够阻断AD发展的预防性治疗方法。靶向多功能以与多种病理成分相互作用的分子被认为可以提高AD的治疗效果。特别是，具有多种作用的草药对AD具有认知益处。补骨M是一种由（鹿茸粉）、地锦草、刺蒺藜和黄芪组成的多草药提取物，其各种成分具有赋予抗认知缺陷能力。
评估补骨M对淀粉样β蛋白（Aβ）毒性及其机制以及对认知功能的潜在作用。
我们阐述了补骨M对Aβ诱发毒性的影响及其减轻大鼠皮质神经元AD发病机制的可能机制。对于认知功能研究，对2月龄雌性3×Tg-AD小鼠给予400mg/kg补骨M，持续30天。进行行为测试以评估补骨M对认知障碍的疗效。
在原代皮质神经元培养中，补骨M通过减少细胞骨架异常和轴突破坏、恢复突触前和突触后蛋白表达、抑制线粒体损伤和凋亡信号以及保留神经发生和神经营养因子来减轻Aβ诱发的毒性。重要的是，给予补骨M 30天可有效预防3月龄雌性3×Tg-AD小鼠认知障碍的发展。
补骨M可能有助于延缓AD的进展，因此其对AD的预防潜力值得考虑。
