The traditional Chinese medicine of Qingxin Kaiqiao Recipe (QKR) is effective in the treatment of Alzheimer's disease (AD). This study aims to investigate whether QKR improves the cognitive ability and takes neuroprotective effect on APP/PS1 double transgenic mice via the PI3K/Akt pathway. APP/PS1 double transgenic mice were randomly divided into a model, donepezil-treated, or QKR-treated group (L-QKR: 4.75 mg/kg/d, M-QKR: 9.5 mg/kg/d, and H-QKR: 19 mg/kg/d, respectively). Wild-type C57/BL6J mice were used as the control group. Morris water maze (MWM) was used to test the ability of spatial navigation and memorization; terminal deoxynucleotidyl transferase-mediated dUTP nick end-labelling (TUNEL) assay was applied to test the apoptosis; amyloid protein granule deposition was detected via Methenamine silver staining; Western blot (WB) analysis, immunohistochemistry, and RT-PCR were applied to measure the expression of A and corresponding indicators of the PI3K/Akt pathway. Compared with the model group, QKR significantly relieved the cognitive impairment, reduced the deposition of senile plaques, decreased the expression of GSK-3 and A, and increased the expression of p-PI3K, p-Akt, and IDE. In addition, the number of TUNEL-positive cells decreased after treatment using QKR. The current study proved that QKR, especially at the high dose tested, exerted a protective effect on improving learning and memory, inhibiting apoptosis, and reducing the process of pathological degeneration in the hippocampus of AD mice.
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http://dx.doi.org/10.1155/2020/3019674 | DOI Listing |
Front Neurosci
November 2024
Department of Rehabilitation Medicine, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Chinese Medicine), Hangzhou, China.
Objective: To examine the effects of long-term aerobic exercise on oxidative stress and learning memory ability of APP/PS1 mice, focusing on the hippocampal Keap1, Nrf2, HO-1, and GPX4 proteins.
Methods: Thirty APP/PS1 double transgenic AD mice were randomly divided into three groups: model group, short-term exercise group, and long-term exercise group, with 10 mice in each group. Male non-transgenic mice of the same age served as the control group.
Immun Inflamm Dis
November 2024
Department of Neurology, Xuan Wu Hospital, Capital Medical University, Beijing, China.
Background: The effectiveness of ultrasound stimulation in treating Alzheimer's disease (AD) has been reported in previous studies, but the underlying mechanisms remain unclear. This study investigated the effects of ultrasound stimulation on the proportion and function of microglia of different phenotypes, as well as on the levels of inflammatory factors. Additionally, it revealed the alterations in proteomic molecules in the mouse hippocampus following ultrasound stimulation treatment, aiming to uncover potential new molecular mechanisms.
View Article and Find Full Text PDFBiol Res
November 2024
Department of Orthopedics, Tongji Hospital, Tongji University School of Medicine, Shanghai, 200065, China.
J Ethnopharmacol
February 2025
Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China; Department of Neurology, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou, China. Electronic address:
Ethnopharmacological Relevance: Alzheimer's disease (AD) is a common type of neurodegenerative disease with the β-amyloid plaques (Aβ) deposition. Previously, Dengzhan Shengmai capsule (DZSM) has been shown to reduce the pathology associated with AD, but the underlying mechanism is unclear.
Aim Of Study: This study investigated the potential mechanisms of DZSM against AD.
Biomaterials
October 2023
School of Life Sciences, Anhui Agricultural University, Hefei, Anhui, 230036, China. Electronic address:
Alzheimer's disease (AD) as a common neurodegenerative disease showed progressive cognitive dysfunction and behavioral impairment. Currently, the deposition of amyloid β-protein (Aβ) remains the main pathomechanism. However, preventing neuronal death induced by Aβ remains elusive, and no effective strategy in clinic was found to combat AD.
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