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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Main Authors: Huijuan Wang, Jun Qian, Xiufen Zhao, Changing Xing, Bin Sun
Format: Article
Language:English
Published: Elsevier 2017-04-01
Series:Journal of Pharmacological Sciences
Subjects:
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.
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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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