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Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation

[Image: see text] Acute liver injury (ALI) and acute kidney injury (AKI) are significantly affected by the antioxidant status. In the present study, the protective effect and mechanism of the collagen peptide Phe-Leu-Ala-Pro (FLAP) in mice with ALI and AKI induced by carbon tetrachloride (CCl(4)) we...

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Autores principales: He, Shuqi, Zhao, Wei, Chen, Xiang, Li, Jie, Zhang, Leifang, Jin, Huoxi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Chemical Society 2022
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753214/
https://www.ncbi.nlm.nih.gov/pubmed/36530242
http://dx.doi.org/10.1021/acsomega.2c04851
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author He, Shuqi
Zhao, Wei
Chen, Xiang
Li, Jie
Zhang, Leifang
Jin, Huoxi
author_facet He, Shuqi
Zhao, Wei
Chen, Xiang
Li, Jie
Zhang, Leifang
Jin, Huoxi
author_sort He, Shuqi
collection PubMed
description [Image: see text] Acute liver injury (ALI) and acute kidney injury (AKI) are significantly affected by the antioxidant status. In the present study, the protective effect and mechanism of the collagen peptide Phe-Leu-Ala-Pro (FLAP) in mice with ALI and AKI induced by carbon tetrachloride (CCl(4)) were examined. The results showed that FLAP effectively improved the liver mass index, the renal mass index, and the histopathological morphology. FLAP treatment significantly decreased the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea nitrogen (BUN), and creatinine (CRE) but increased the activity of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). The protein expression levels of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), p-protein kinase B (p-AKT), and p-phosphatidylinositol-3-kinase (p-PI3K) in the liver and kidneys were significantly up-regulated after FLAP treatment. FLAP down-regulated the levels of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), and nuclear factor-κ B (NF-κB) in liver and kidney tissues. Thus, FLAP may play a protective role in ALI and AKI by attenuating oxidative stress and inflammation mediated by the Nrf2/anti-response element (ARE) and PI3K/AKT/NF-κB pathways.
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spelling pubmed-97532142022-12-16 Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation He, Shuqi Zhao, Wei Chen, Xiang Li, Jie Zhang, Leifang Jin, Huoxi ACS Omega [Image: see text] Acute liver injury (ALI) and acute kidney injury (AKI) are significantly affected by the antioxidant status. In the present study, the protective effect and mechanism of the collagen peptide Phe-Leu-Ala-Pro (FLAP) in mice with ALI and AKI induced by carbon tetrachloride (CCl(4)) were examined. The results showed that FLAP effectively improved the liver mass index, the renal mass index, and the histopathological morphology. FLAP treatment significantly decreased the levels of serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea nitrogen (BUN), and creatinine (CRE) but increased the activity of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). The protein expression levels of nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), p-protein kinase B (p-AKT), and p-phosphatidylinositol-3-kinase (p-PI3K) in the liver and kidneys were significantly up-regulated after FLAP treatment. FLAP down-regulated the levels of interleukin-6 (IL-6), IL-1β, tumor necrosis factor-α (TNF-α), and nuclear factor-κ B (NF-κB) in liver and kidney tissues. Thus, FLAP may play a protective role in ALI and AKI by attenuating oxidative stress and inflammation mediated by the Nrf2/anti-response element (ARE) and PI3K/AKT/NF-κB pathways. American Chemical Society 2022-12-02 /pmc/articles/PMC9753214/ /pubmed/36530242 http://dx.doi.org/10.1021/acsomega.2c04851 Text en © 2022 The Authors. Published by American Chemical Society https://creativecommons.org/licenses/by-nc-nd/4.0/Permits non-commercial access and re-use, provided that author attribution and integrity are maintained; but does not permit creation of adaptations or other derivative works (https://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle He, Shuqi
Zhao, Wei
Chen, Xiang
Li, Jie
Zhang, Leifang
Jin, Huoxi
Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation
title Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation
title_full Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation
title_fullStr Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation
title_full_unstemmed Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation
title_short Ameliorative Effects of Peptide Phe-Leu-Ala-Pro on Acute Liver and Kidney Injury Caused by CCl(4) via Attenuation of Oxidative Stress and Inflammation
title_sort ameliorative effects of peptide phe-leu-ala-pro on acute liver and kidney injury caused by ccl(4) via attenuation of oxidative stress and inflammation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9753214/
https://www.ncbi.nlm.nih.gov/pubmed/36530242
http://dx.doi.org/10.1021/acsomega.2c04851
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