Gu Xinru, Zhao Haiyu, Zhou Junyi, Zhou Yanyan, Wei Xiaolu, Wang Hongjie, Bian Baolin, Yang Jian, Ren Wei, Si Nan
Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences, Beijing 100700, China.
Drug Research Center of Integrated Traditional Chinese and Western Medicine, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou 646000, China.
Evid Based Complement Alternat Med. 2020 Jan 2;2020:6212907. doi: 10.1155/2020/6212907. eCollection 2020.
Huang-Lian-Jie-Du Decoction (HLJDD), traditional Chinese medicine (TCM), is proven to have ameliorative effects on learning and memory deficits of Alzheimer's disease (AD). The current study aims to reveal the underlying mechanism of HLJDD in the treatment of AD by simultaneous determination on the regulation of HLJDD on oxidative stress, neurotransmitters, and AMPK-SIRT1 pathway in AD. AD model rat was successfully established by injection of D-galactose and A -ibotenic acid. Morris Water Maze (MWM) test was used to evaluate the success of AD modelling. On this basis, an advanced technique with UPLC-QqQ MS/MS was built up and applied to determine the levels of 8 neurotransmitters in rat plasma. Significant alternation in methionine, glutamine, and tryptophan was observed in AD rats' plasma after the administration of HLJDD, relative to the model group. Meanwhile, HLJDD could upregulate the levels of SOD, GSH-Px, AMPK, and SIRT1 and downregulate the content of MDA in the peripheral system of the AD rats. The underlying therapeutic mechanism of HLJDD for the treatment of AD was associated with alleviating oxidation stress, inflammation, neurotransmitters, and energy metabolism. These data provide solid foundation for the potential use of HLJDD to treat AD.
黄连解毒汤（HLJDD）作为一种传统中药，已被证明对阿尔茨海默病（AD）的学习和记忆缺陷具有改善作用。本研究旨在通过同时测定HLJDD对AD氧化应激、神经递质和AMPK-SIRT1通路的调节作用，揭示其治疗AD的潜在机制。通过注射D-半乳糖和A-鹅膏蕈氨酸成功建立AD模型大鼠。采用Morris水迷宫（MWM）试验评估AD建模的成功与否。在此基础上，建立了一种先进的超高效液相色谱-串联四极杆质谱联用（UPLC-QqQ MS/MS）技术，并用于测定大鼠血浆中8种神经递质的水平。与模型组相比，给予HLJDD后，AD大鼠血浆中的蛋氨酸、谷氨酰胺和色氨酸有显著变化。同时，HLJDD可上调AD大鼠外周系统中SOD、GSH-Px、AMPK和SIRT1的水平，并下调MDA的含量。HLJDD治疗AD的潜在机制与减轻氧化应激、炎症、神经递质和能量代谢有关。这些数据为HLJDD治疗AD的潜在应用提供了坚实的基础。
