Dipeptide IF prevents the effects of hypertension‐induced Alzheimer's disease on long‐term memory in the cortex of spontaneously hypertensive rats

Hypertension (HTN) is one of the most prevalent chronic conditions; it can damage blood vessels and rupture blood vessels can trap in small vessels. This blockage can prevent blood flow and oxygen delivery to brain cells and can result in Alzheimer's disease (AD). HTN‐ and AD‐mediated long‐time...

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Veröffentlicht in:Environmental toxicology 2020-05, Vol.35 (5), p.570-581
Hauptverfasser: Chang, Yung‐Ming, Ashok Kumar, K., Ju, Da‐Tong, Ho, Tsung‐Jung, Mahalakshmi, B., Lin, Wan‐Teng, Day, Cecilia H., Vijaya Padma, V., Liao, Po‐Hsiang, Huang, Chih‐Yang
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Sprache:eng
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Zusammenfassung:Hypertension (HTN) is one of the most prevalent chronic conditions; it can damage blood vessels and rupture blood vessels can trap in small vessels. This blockage can prevent blood flow and oxygen delivery to brain cells and can result in Alzheimer's disease (AD). HTN‐ and AD‐mediated long‐time memory loss and its treatment remain poorly understood. Plant‐derived natural compounds are alternative solutions for effectively treating diseases without any side effects. This study revealed that bioactive peptides extracted from potato hydrolysis suppress HTN‐mediated long‐term memory (LTM) loss and cell apoptosis, thus improving memory formation and neuronal cell survival in the spontaneously hypertensive rat (SHR) rat model. SHR rats were treated with bioactive peptide IF (10 mg/kg orally) and angiotensin‐converting enzyme inhibitors (5 mg/kg orally). In this study, we evaluated the molecular expression levels of BDNF‐, GluR1‐, and CREB‐mediated markers protein expression in 24‐week‐old SHR rats. The study result showed that HTN‐induced AD regulated long‐term memory (LTM) loss and neuronal degeneration in the SHR animals. The bioactive peptide‐treated animals showed an elevated level of survival proteins. Bioactive peptide IF activate CREB‐mediated downstream proteins to regulate synaptic plasticity and neuronal survival in the SHR rat model.
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.22892