Ko Yong-Hyun, Kwon Seung-Hwan, Hwang Ji-Young, Kim Kyung-In, Seo Jee-Yeon, Nguyen Thi-Lien, Lee Seok-Yong, Kim Hyoung-Chun, Jang Choon-Gon
Department of Pharmacology, School of Pharmacy, Sungkyunkwan University, Suwon 16419, Republic of Korea.
Department of Pharmacology, National Institute of Drug Quality Control, 48-Hai Ba Trung, Ha Noi, Viet Nam.
Biomol Ther (Seoul). 2018 Mar 1;26(2):109-114. doi: 10.4062/biomolther.2016.284.
Liquiritigenin (LQ) is a flavonoid that can be isolated from radix. It is frequently used as a tranditional oriental medicine herbal treatment for swelling and injury and for detoxification. However, the effects of LQ on cognitive function have not been fully explored. In this study, we evaluated the memory-enhancing effects of LQ and the underlying mechanisms with a focus on the N-methyl-D-aspartic acid receptor (NMDAR) in mice. Learning and memory ability were evaluated with the Y-maze and passive avoidance tests following administration of LQ. In addition, the expression of NMDAR subunits 1, 2A, and 2B; postsynaptic density-95 (PSD-95); phosphorylation of Ca/calmodulin-dependent protein kinase II (CaMKII); phosphorylation of extracellular signal-regulated kinase 1/2 (ERK 1/2); and phosphorylation of cAMP response element binding (CREB) proteins were examined by Western blot. , we found that treatment with LQ significantly improved memory performance in both behavioral tests. , LQ significantly increased NMDARs in the hippocampus. Furthermore, LQ significantly increased PSD-95 expression as well as CaMKII, ERK, and CREB phosphorylation in the hippocampus. Taken together, our results suggest that LQ has cognition enhancing activities and that these effects are mediated, in part, by activation of the NMDAR and CREB signaling pathways.
甘草素（LQ）是一种可从甘草中分离出来的黄酮类化合物。它常被用作传统东方草药疗法，用于消肿、疗伤和解毒。然而，LQ对认知功能的影响尚未得到充分研究。在本研究中，我们评估了LQ对小鼠的记忆增强作用及其潜在机制，重点关注N-甲基-D-天冬氨酸受体（NMDAR）。在给予LQ后，通过Y迷宫和被动回避试验评估学习和记忆能力。此外，通过蛋白质免疫印迹法检测NMDAR亚基1、2A和2B、突触后致密蛋白95（PSD-95）、钙/钙调蛋白依赖性蛋白激酶II（CaMKII）的磷酸化、细胞外信号调节激酶1/2（ERK 1/2）的磷酸化以及环磷酸腺苷反应元件结合蛋白（CREB）的磷酸化。我们发现，在两项行为测试中，LQ治疗均显著改善了记忆表现。此外，LQ显著增加了海马体中的NMDAR。此外，LQ显著增加了海马体中PSD-95的表达以及CaMKII、ERK和CREB的磷酸化。综上所述，我们的结果表明，LQ具有认知增强活性，且这些作用部分是由NMDAR和CREB信号通路的激活介导的。
