Dexmedetomidine Provides Protection Against Hippocampal Neuron Apoptosis and Cognitive Impairment in Mice with Alzheimer
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Dexmedetomidine Provides Protection Against Hippocampal Neuron Apoptosis and Cognitive Impairment in Mice with Alzheimer’s Disease by Mediating the miR-129/YAP1/JAG1 Axis Weiying Sun 1 & Jun Zhao 2 & Chunzhi Li 1 Received: 24 March 2020 / Accepted: 10 August 2020 # Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Alzheimer’s disease (AD) is a multifactorial neurodegenerative disease that leads to progressive cognitive, memory, and learning dysfunction that affects the aging population. Dexmedetomidine (Dex) might be beneficial for postoperative cognitive function in elderly patients. However, the exact mechanism underlying the protective role of Dex against cognitive impairment requires further elucidation. The present study aims to determine whether miR-129 is involved in the protective effect of Dex against Aβ1– 42-induced hippocampal neuron apoptosis and cognitive impairment in mice. In our study, Y-shaped maze and water maze tests were conducted to evaluate the cognitive function of AD mice, while neuronal apoptosis was measured by Terminal Deoxynucleotidyl Transferase–Mediated dUTP Nick-End Labeling (TUNEL) staining. The findings showed that Dex administration resulted in the enhancement of miR-129 expression with declined hippocampal neuron apoptosis and attenuated cognitive impairment in Aβ1–42-injected mice. miR-129 targeted YAP1 and disrupted its interaction with JAG1, leading to a decline in hippocampal neuron apoptosis and attenuated cognitive impairment in Aβ1–42-injected mice. In conclusion, the miR-129/YAP1/ JAG1 axis could potentially be the mechanism by which Dex protects AD mice from cognitive impairment. Keywords Dexmedetomidine . microRNA-129 . Yes-associated protein 1/Jagged 1 signaling pathway . Alzheimer’s disease . Neurons . Cognitive function
Introduction Alzheimer’s disease (AD) is the most prevalent neurodegenerative diseases that has placed significant burden on the health care system in both developed and developing countries [1]. AD strips people the patients of their independence due to the remarkable cognitive, behavioral, and psychological deficits it results [2]. The deposition of amyloid-beta (Aβ) peptides into amyloid plaques contributes to the development of cognitive dysfunction in AD [3]. Hippocampal atrophy has also been reported to be linked to cognitive malfunction in AD [4]. At present, there is no drug that can slow the progression of AD, much less permanently cure the disease. * Chunzhi Li [email protected] 1
Department of Pharmacy, Linyi People’s Hospital, No. 27, Jiefang East Road, Lanshan District, Linyi 276000, Shandong Province, People’s Republic of China
2
Department of Ophthalmology, Linyi People’s Hospital, Linyi 276000, People’s Republic of China
Dexmedetomidine (Dex) is an α2-adrenoceptor agonist with high selectivity, which provides sedative, analgesic, and opioid-sparing clinical outcomes [5]. The antiinflammatory and neuroprotective roles of Dex have been illustrated in previous animal studies [6]. Dex has been reported to
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