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  4. The antifibrotic and anti-inflammatory effects of icariin on the kidney in a unilateral ureteral obstruction mouse model
 
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The antifibrotic and anti-inflammatory effects of icariin on the kidney in a unilateral ureteral obstruction mouse model

Journal
Phytomedicine
Journal Volume
59
Date Issued
2019
Author(s)
Chen H.A.
CHANG-MU CHEN  
Guan S.-S.
CHIH-KANG CHIANG  
Wu C.-T.
SHING-HWA LIU  
DOI
10.1016/j.phymed.2019.152917
URI
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85064081831&doi=10.1016%2fj.phymed.2019.152917&partnerID=40&md5=c31e8c0d805619e744247fe9140896ea
https://scholars.lib.ntu.edu.tw/handle/123456789/431126
Abstract
Background: The pathology change of renal tubulointerstitial fibrosis is a critical feature of chronic kidney disease (CKD), regardless of the primary insults. The infiltration of inflammatory cells and the consecutive secretion of profibrotic factors are frequently and conspicuously observed during the development of renal fibrosis. Icariin, an active polyphenol of the Epimedium genus, has been found to alleviate the symptoms of chronic diseases like diabetes, neurodegeneration, and heart and renal diseases. The effect and mechanism of icariin on the prevention of CKD-associated renal fibrosis still needed clarification. Purpose: The aims of this study were to investigate whether icariin treatment improves the development of CKD-associated renal fibrosis and its possible mechanism. Methods: An experimental unilateral ureteral obstruction (UUO)-induced chronic renal fibrosis mouse model was used. Mice were orally administered with icariin (20 mg/kg/day) for 3 consecutive days before and 14 consecutive days after UUO surgery. Results: The pathological changes, collagen deposition, and protein expressions of profibrotic factors (transforming growth factor-β and connective tissue growth factor) and fibrotic markers (α-smooth muscle actin and fibronectin), which were significantly elevated in the kidneys of UUO mice, could be significantly reversed by icariin treatment. Icariin treatment also significantly inhibited the increased Smad2/3 and decreased E-cadherin protein expressions in the kidneys of UUO mice. Icariin treatment prominently mitigated the protein expression of proinflammatory factors like nuclear factor-κB, cyclooxygenase-2, interleukin 1-β and prooxidative enzyme (NADPH oxidase-4), and it increased the protein expression of antioxidative enzymes (superoxide dismutase and catalase). Conclusion: Icariin treatment protects against CKD-associated renal fibrosis via its antifibrotic and anti-inflammatory properties. Icariin may serve as a therapeutic agent in the prevention of CKD-associated renal fibrosis. ? 2019 Elsevier GmbH
SDGs

[SDGs]SDG3

Other Subjects
alpha smooth muscle actin; candesartan; catalase; collagen; connective tissue growth factor; copper zinc superoxide dismutase; cyclooxygenase 2; fibronectin; icariin; immunoglobulin enhancer binding protein; interleukin 1beta; reactive oxygen metabolite; reduced nicotinamide adenine dinucleotide phosphate oxidase 4; transforming growth factor beta; uvomorulin; antiinflammatory agent; collagen; fibronectin; flavonoid; icariin; transforming growth factor beta; adult; animal cell; animal experiment; animal model; animal tissue; antifibrotic activity; antiinflammatory activity; Article; cell infiltration; controlled study; granulocyte; immunohistochemistry; mouse; mouse model; nonhuman; obstruction-induced renal fibrosis; oxidative stress; priority journal; protein expression; animal; complication; disease model; drug effect; fibrosis; kidney; kidney disease; male; metabolism; ureter obstruction; Animals; Anti-Inflammatory Agents; Collagen; Disease Models, Animal; Fibronectins; Fibrosis; Flavonoids; Kidney; Kidney Diseases; Male; Mice; Transforming Growth Factor beta; Ureteral Obstruction
Publisher
Elsevier GmbH
Type
journal article

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