Department of Pharmacy, Gansu Provincial People's Hospital.
School of Pharmacy, Gansu University of Traditional Chinese Medicine, Lanzhou, China.
Neuroreport. 2023 Dec 6;34(17):825-833. doi: 10.1097/WNR.0000000000001960. Epub 2023 Oct 17.
Alzheimer's disease (AD) is a degenerative disorder characterized by cognitive dysfunction and BDNF/TrkB is a well-conceived anti-AD signaling. Cynomorium songaricum Rupr. ( C. songaricum ) is a herb with promising neuroprotective effects and the function is majorly attributed to flavonoids. The current study attempted to explore the effects of total flavonoids of C. songaricum (CS) on AD model by focusing on changes in BDNF/TrkB axis. AD model was induced in rats via transcranial injection of Aβ 1-42 and AD symptoms treated with CS of three doses. Donepezil was used as the positive control. Changes in rat memory and learning abilities, brain histological, apoptosis, production of neurotransmitters, BDNF/TrkB axis, and apoptosis-related markers were measured. The injection of Aβ 1-42 induced cognitive dysfunction in AD rats. The integrity of brain tissue structure was destructed and apoptosis was induced in AD rats, in which was found the increased production of AChE and Aβ 1-42 , and decreased production of ChAT, ACH. At the molecular level, the expression of BDNF, TrkB, and Bcl-2 was suppressed, while the expression of Bax, caspase-3, and caspase-9 was induced. After the administration of CS, the memory and learning abilities of rats were improved, the production of neurotransmitter was restored, ordered arrangement of pyramidal cells was retained, and neuron apoptosis was inhibited. The attenuation of Aβ 1-42 -indcued impairments was associated with the activation of BDNF/TrkB axis and blockade of apoptosis-related pathways. Collectively, CS can improve learning and memory abilities in Aβ 1-42 -induced AD model rats. which may depend on the activation of the hippocampal BDNF/TrkB signaling pathway.
阿尔茨海默病（AD）是一种以认知功能障碍为特征的退行性疾病，BDNF/TrkB 是一种合理的抗 AD 信号。肉苁蓉（C. songaricum）是一种具有神经保护作用的草药，其功能主要归因于类黄酮。本研究试图通过关注 BDNF/TrkB 轴的变化，探讨肉苁蓉总黄酮（CS）对 AD 模型的影响。通过跨颅注射 Aβ 1-42 诱导大鼠 AD 模型，并采用三种剂量的 CS 治疗 AD 症状。多奈哌齐用作阳性对照。测量大鼠记忆和学习能力、脑组织学、细胞凋亡、神经递质产生、BDNF/TrkB 轴和细胞凋亡相关标志物的变化。Aβ 1-42 的注射诱导 AD 大鼠认知功能障碍。AD 大鼠脑组织结构完整性被破坏并诱导细胞凋亡，其中发现 AChE 和 Aβ 1-42 的产生增加，ChAT、ACH 的产生减少。在分子水平上，BDNF、TrkB 和 Bcl-2 的表达受到抑制，而 Bax、caspase-3 和 caspase-9 的表达受到诱导。CS 给药后，大鼠的记忆和学习能力得到改善，神经递质的产生得到恢复，锥体细胞的有序排列得到保留，神经元凋亡得到抑制。CS 对 Aβ 1-42 诱导损伤的衰减与 BDNF/TrkB 轴的激活和凋亡相关途径的阻断有关。总之，CS 可改善 Aβ 1-42 诱导的 AD 模型大鼠的学习和记忆能力，这可能依赖于海马 BDNF/TrkB 信号通路的激活。
