β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis
Renal fibrosis is a hallmark feature of chronic kidney disease, which is reflected by proliferation and migration of interstitial fibroblasts and extracellular matrix (ECM) accumulation. β-Aminoisobutyric acid (BAIBA) is recently demonstrated to exert a protective role from metabolic diseases. Howev...
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Elsevier
2017-04-01
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Series: | Journal of Pharmacological Sciences |
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Online Access: | http://www.sciencedirect.com/science/article/pii/S1347861317300038 |
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author | Huijuan Wang Jun Qian Xiufen Zhao Changing Xing Bin Sun |
author_facet | Huijuan Wang Jun Qian Xiufen Zhao Changing Xing Bin Sun |
author_sort | Huijuan Wang |
collection | DOAJ |
description | Renal fibrosis is a hallmark feature of chronic kidney disease, which is reflected by proliferation and migration of interstitial fibroblasts and extracellular matrix (ECM) accumulation. β-Aminoisobutyric acid (BAIBA) is recently demonstrated to exert a protective role from metabolic diseases. However, whether and how BAIBA on fibroblast activation and renal fibrosis response to angiotensin II (Ang II) remains largely obscure. Herein, we showed that BAIBA significantly depressed the proliferation and migration of NRK-49F cells in vitro. Treatment with Ang II remarkably up-regulated the expressions of fibronectin (FN), collagen 1 (COL 1), α-smooth muscle actin (α-SMA), interleukin-17 (IL-17) and nicotinamide adenine dinucleotide phosphate oxidase (NOX2)-derived reactive oxygen species (ROS) production in cultured NRK-49F cells. Pretreatment with BAIBA almost blocked Ang II-induced ECM production and IL-17-mediated oxidative stress in NRK-49F cells. BAIBA treatment ameliorates fibroblasts activation and renal fibrosis in rat obstructed kidneys involving inhibition of Ang II/IL-17/ROS signaling transduction, which may be considered as a therapeutic candidate for fibrosis-related diseases. |
first_indexed | 2024-12-13T04:08:47Z |
format | Article |
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issn | 1347-8613 |
language | English |
last_indexed | 2024-12-13T04:08:47Z |
publishDate | 2017-04-01 |
publisher | Elsevier |
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series | Journal of Pharmacological Sciences |
spelling | doaj.art-193475fb3d2243948f23af94052af2ae2022-12-22T00:00:07ZengElsevierJournal of Pharmacological Sciences1347-86132017-04-01133420321310.1016/j.jphs.2016.12.005β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosisHuijuan Wang0Jun Qian1Xiufen Zhao2Changing Xing3Bin Sun4Department of Immunology, Nanjing Medical University, Nanjing, Jiangsu Province, 210029, ChinaDepartment of Nephrology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu Province, 210029, ChinaDepartment of Nephrology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu Province, 210029, ChinaDepartment of Nephrology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu Province, 210029, ChinaDepartment of Nephrology, The First Affiliated Hospital with Nanjing Medical University, Nanjing, Jiangsu Province, 210029, ChinaRenal fibrosis is a hallmark feature of chronic kidney disease, which is reflected by proliferation and migration of interstitial fibroblasts and extracellular matrix (ECM) accumulation. β-Aminoisobutyric acid (BAIBA) is recently demonstrated to exert a protective role from metabolic diseases. However, whether and how BAIBA on fibroblast activation and renal fibrosis response to angiotensin II (Ang II) remains largely obscure. Herein, we showed that BAIBA significantly depressed the proliferation and migration of NRK-49F cells in vitro. Treatment with Ang II remarkably up-regulated the expressions of fibronectin (FN), collagen 1 (COL 1), α-smooth muscle actin (α-SMA), interleukin-17 (IL-17) and nicotinamide adenine dinucleotide phosphate oxidase (NOX2)-derived reactive oxygen species (ROS) production in cultured NRK-49F cells. Pretreatment with BAIBA almost blocked Ang II-induced ECM production and IL-17-mediated oxidative stress in NRK-49F cells. BAIBA treatment ameliorates fibroblasts activation and renal fibrosis in rat obstructed kidneys involving inhibition of Ang II/IL-17/ROS signaling transduction, which may be considered as a therapeutic candidate for fibrosis-related diseases.http://www.sciencedirect.com/science/article/pii/S1347861317300038β-Aminoisobutyric acidAngiotensin IIExtracellular matrixInterleukin-17Reactive oxygen species |
spellingShingle | Huijuan Wang Jun Qian Xiufen Zhao Changing Xing Bin Sun β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis Journal of Pharmacological Sciences β-Aminoisobutyric acid Angiotensin II Extracellular matrix Interleukin-17 Reactive oxygen species |
title | β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis |
title_full | β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis |
title_fullStr | β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis |
title_full_unstemmed | β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis |
title_short | β-Aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis |
title_sort | β aminoisobutyric acid ameliorates the renal fibrosis in mouse obstructed kidneys via inhibition of renal fibroblast activation and fibrosis |
topic | β-Aminoisobutyric acid Angiotensin II Extracellular matrix Interleukin-17 Reactive oxygen species |
url | http://www.sciencedirect.com/science/article/pii/S1347861317300038 |
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