Abstract
Hypertension is one of the growing risk factors for the progression of long-term memory loss. Hypertension-mediated memory loss and treatment remain not thoroughly elucidated to date. Plant-based natural compounds are an alternative solution to treating human diseases without side effects associated with commercial drugs. This study reveals that bioactive peptides extracted from soy hydrolysates mimic hypertension-mediated memory loss and neuronal degeneration and alters the memory molecular pathway in spontaneously hypertensive rats (SHR). The SHR animal model was treated with bioactive peptide VHVV (10 mg/kg/oral administration) and angiotensin-converting-enzyme (ACE) inhibitors (5 mg/kg/oral administration) for 24 weeks. We evaluated molecular level expression of brain-derived neurotrophic factor (BDNF), cAMP response element binding protein (CREB), and survival markers phospho-protein kinase B (P-AKT) and phosphoinositide 3-kinase (PI3K) after 24 weeks of treatment for SHR in this study. Western blotting, hematoxylin and eosin (H&E) staining, and immunohistochemistry showed long-term memory loss and neuronal degeneration in SHR animals. Bioactive peptide VHVV-treated animals upregulated the expression of long-term memory-relate proteins and neuronal survival. Spontaneously hypertensive rats treated with oral administration of bioactive peptide VHVV had activated CREB-mediated downstream proteins which may reduce hypertension-mediated long-term memory loss and maintain neuronal survival.
Highlights
Hypertension-mediated health problems are a major problem in the Western world
We found that the downstream protein of brain-derived neurotrophic factor (BDNF) was expressed more in the bioactive peptide VHVV-treated animals, which was confirmed with immunohistochemical assay, and we concluded that our bioactive peptide VHVV potentially increased memory formation and neuronal cell survival by way of the overexpression of BDNF
According to the histopathological results, we hypothesized that hypertension affects memory formation and alters the structural and functional changes in the rat cortex similar to how the bioactive peptide VHVV reverses hypertension-mediated neuronal degeneration and structural and functional changes (Figure 1). We found that both BDNF-Glutamate R-1 and tropomyosin receptor kinase B (TrkB)-phosphoinositide 3-kinase (PI3K) mediated signaling pathways are involved in long-term memory formation and cell survival through bioactive peptide VHVV
Summary
Hypertension-mediated health problems are a major problem in the Western world. Hypertension causes a series of diseases in the brain, heart, and kidneys. The molecular proteins that are responsible for neuronal cell survival, such as PI3K-AKT-mTOR, were expressed more in the bioactive peptide VHVV-treated group compared to the SHR and ACE-treated animals. According to the histopathological results, we hypothesized that hypertension affects memory formation and alters the structural and functional changes in the rat cortex similar to how the bioactive peptide VHVV reverses hypertension-mediated neuronal degeneration and structural and functional changes (Figure 1). We found that both BDNF-Glutamate R-1 and TrkB-PI3K mediated signaling pathways are involved in long-term memory formation and cell survival through bioactive peptide VHVV. It is suggested that the expression of BDNF in the cortex is a more effective way to approach hypertension-mediated defects
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