Heo Jae-Jun, Han Young-Eun, Kim Min Soo, Cheong Eunji, Choi Chun Whan, Oh Soo-Jin
Brain Science Institute, Korea Institute of Science and Technology (KIST), Seoul, Republic of Korea.
Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, Seoul, Republic of Korea.
Phytother Res. 2025 Feb;39(2):593-603. doi: 10.1002/ptr.8395. Epub 2024 Nov 25.
Monoamine oxidase B (MAO-B) has emerged as a therapeutic target for Alzheimer's disease (AD) due to its involvement in the synthesis of γ-aminobutyric acid (GABA) in reactive astrocytes, which inhibits neuronal activity. Suffruticosol B (Suf-B), isolated from Paeonia lactiflora, is one of the resveratrol oligomers. Although resveratrol oligomers have demonstrated neuroprotective effects, it remains unexplored whether Suf-B exerts therapeutic effects on AD by targeting MAO-B. In this study, we investigated whether Suf-B alleviates AD pathology by mitigating reactive astrogliosis and inhibiting the overproduction of astrocytic GABA. After confirming the MAO-B inhibitory effect of Suf-B through MAO-B enzyme assay, we administered Suf-B to APP/PS1 AD model mice. To test the potential therapeutic action of Suf-B in AD, a series of experiments were conducted, including behavioral tests such as the open field test, novel object recognition test, Barnes maze test, passive avoidance test, as well as immunohistochemistry and whole-cell patch-clamp recordings. We found that Suf-B markedly inhibited MAO-B activity without causing cytotoxicity. Immunohistochemistry and electrophysiology experiments demonstrated that Suf-B significantly reduced astrocyte reactivity, as well as an aberrant increase in GABA production and tonic GABA release from astrocytes in AD. Behavior test results indicated that Suf-B treatment restored cognitive function in APP/PS1 mice. In conclusion, Suf-B effectively reduces excessive GABA production in reactive astrocytes by inhibiting MAO-B, normalizing aberrant inhibition in hippocampal neurons in an AD mouse model. These results suggest that Suf-B has potential as a treatment for AD and may be applicable to other brain diseases associated with reactive astrogliosis.
单胺氧化酶B(MAO-B)已成为阿尔茨海默病(AD)的治疗靶点,因为它参与反应性星形胶质细胞中γ-氨基丁酸(GABA)的合成,从而抑制神经元活动。从芍药中分离出的紫铆素B(Suf-B)是白藜芦醇低聚物之一。尽管白藜芦醇低聚物已显示出神经保护作用,但Suf-B是否通过靶向MAO-B对AD发挥治疗作用仍未得到探索。在本研究中,我们调查了Suf-B是否通过减轻反应性星形胶质细胞增生和抑制星形胶质细胞GABA的过度产生来减轻AD病理。通过MAO-B酶测定证实Suf-B对MAO-B的抑制作用后,我们将Suf-B给予APP/PS1 AD模型小鼠。为了测试Suf-B在AD中的潜在治疗作用,我们进行了一系列实验,包括行为测试,如旷场试验、新物体识别试验、巴恩斯迷宫试验、被动回避试验,以及免疫组织化学和全细胞膜片钳记录。我们发现Suf-B显著抑制MAO-B活性而不引起细胞毒性。免疫组织化学和电生理实验表明,Suf-B显著降低了星形胶质细胞的反应性,以及AD中星形胶质细胞GABA产生和紧张性GABA释放的异常增加。行为测试结果表明,Suf-B治疗恢复了APP/PS1小鼠的认知功能。总之,Suf-B通过抑制MAO-B有效减少反应性星形胶质细胞中过量的GABA产生,使AD小鼠模型海马神经元的异常抑制正常化。这些结果表明,Suf-B具有治疗AD的潜力,可能适用于与反应性星形胶质细胞增生相关的其他脑部疾病。