Ranuncoside’s attenuation of scopolamine-induced memory impairment in mice via Nrf2 and NF-ĸB signaling

Sara Salahuddin, Hafiza; Attaullah, Sobia; Ali Shah, Shahid; Khan, SanaUllah; Zahid, Muhammad; Ullah, Mujeeb; Khayyam,; Salahuddin, Sidra; Gul, Seema; Alsugoor, Mahdi H

doi:10.1016/j.jsps.2023.101702

Cited by 2 publications

(1 citation statement)

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“…Alzheimer's disease (AD) is an aged-related neurodegenerative disorder characterized by progressive memory loss (Du et al 2020; Ko et al 2019; Zhang et al 2022). Numerous studies have shown that senile plaques, amyloid-β plaques, in ammation, and oxidative stress processes can cause cognitive and memory impairments in central nervous system (Sara et al 2023; Sheppard and Coleman 2020). In addition, cholinergic neurons regulate several nuclei in the brain through neurotransmission and participate in assorted physiological activities such as learning and memory, attention, emotion, and movement, and the loss and degeneration of cholinergic neurotransmitters can induce cognitive impairment (He et al 2023).…”

Section: Introductionmentioning

confidence: 99%

Safflower Yellow Alleviates Cognitive Impairment in Mice by Modulating Cholinergic System Function, Oxidative Stress, and CREB/BDNF/TrkB Signaling Pathway

qi,

wang,

et al. 2024

Preprint

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Alzheimer's disease (AD) is a progressive neurodegenerative disease that primarily develops in old age. The main clinical symptom of the disease is memory loss. Therefore, the treatment of learning and memory dysfunction is an important research direction for prevention and treatment of AD. Studies have shown that scopolamine hydrobromide (SCOP), sodium nitrite (NaNO2) and ethanol impair memory acquisition, memory consolidation and memory retrieval in mice, respectively. Safflower yellow (SY) can effectively improve the memory function of AD mice, but the specific mechanism needs further exploration. In the present study, mice were injected with SCOP, NaNO2 and 40% ethanol to establish models of memory acquisition, memory consolidation and memory retrieval impairment. This study investigated the mechanism of SY treatment of AD from the perspectives of oxidative stress, the cholinergic system, the CREB/BDNF/TrkB signaling pathway and synaptic protein expression. We conducted several studies that have shown that after SY treatment, the memory ability of three memory impairment mice models improved, the pathological changes in brain tissue were reduced, the activity of cholinergic system-related enzymes were changed, the level of oxidative stress in the brain of mice was reduced, and the CREB/BDNF/TrkB pathway was activated. In addition, SY can also upregulate the expression of synapse-associated proteins and exert neuroprotective effects.

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