The soybean bioactive peptide VHVV alleviates hypertension-induced renal damage in hypertensive rats via the SIRT1-PGC1α/Nrf2 pathway
[Display omitted] •The peptide VHVV may suppress hypertensive renal damage.•Changes in the hypertensive kidney were restored by VHVV.•VHVV modulated oxidant defense mechanisms in the hypertensive kidney.•The cellular mitochondrial equilibrium in the SHR kidney was maintained by VHVV.•SIRT1-PGC1α/Nrf...
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Published in | Journal of functional foods Vol. 75; p. 104255 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Elsevier Ltd
01.12.2020
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | [Display omitted]
•The peptide VHVV may suppress hypertensive renal damage.•Changes in the hypertensive kidney were restored by VHVV.•VHVV modulated oxidant defense mechanisms in the hypertensive kidney.•The cellular mitochondrial equilibrium in the SHR kidney was maintained by VHVV.•SIRT1-PGC1α/Nrf2 were activated by VHVV, enhancing ROS scavenging in SHR kidney.
Hypertension triggers oxidative stress, causing dysfunction in organs, including the brain, heart, and kidney. In this study, we examined the potential renal benefit of the soybean bioactive peptide VHVV by in silico analysis and in spontaneously hypertensive rats. Sixteen-week-old spontaneously hypertensive rats were divided into 3 groups and treated with or without VHVV or captopril. Age-matched Wistar-Kyoto rats were used as normotensive control group. The rats were sacrificed after 8 weeks of treatment, and kidneys were analyzed to demonstrate the efficacy of VHVV. In silico analysis confirmed the antihypertensive activity of VHVV. In animal study, VHVV induced antioxidant defense and modulated mitochondrial homeostasis in the hypertensive kidney via SIRT1-PGC1α/Nrf2 pathway. Hence, improvements in renal cells were attributed to the suppression of inflammation and apoptosis, and the architecture of the hypertensive kidney was restored after peptide treatment. Overall, VHVV exhibited therapeutic effects by decreasing renal damage caused by hypertension-induced free radicals. |
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ISSN: | 1756-4646 2214-9414 |
DOI: | 10.1016/j.jff.2020.104255 |