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      Osthole decreases collagen I /III contents and their ratio in TGF- β1-overexpressed mouse cardiac fibroblasts through regulating the TGF- β/Smad signaling pathway

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          Abstract

          The present study was designed to elucidate whether the mechanism by which osthole decreases collagen I / III contents and their ratio is regulating the TGF- β/Smad signaling pathway in TGF- β1-overexpressed mouse cardiac fibroblasts (CFs). These CFs were cultured and treated with different concentrations of osthole. Our results showed that the TGF- β1 expression in the CFs transfected with that the recombinant expression plasmids pcDNA3.1(+)-TGF- β1 was significantly enhanced. After the CFs were treated with 1.25–5 μg-mL –1 of osthole for 24 h, the mRNA and protein expression levels of collagens I and III were reduced. The collagen I / III ratio was also reduced. The mRNA and protein expression levels of TGF- β1, TβR I , Smad2/3, P-Smad2/3, Smad4, and α-SMA were decreased, whereas the expression level of Smad7 was increased. These effects suggested that osthole could inhibit collagen I and III expression and reduce their ratio via the TGF- β/Smad signaling pathway in TGF- β1 overexpressed CFs. These effects of osthole may play beneficial roles in the prevention and treatment of myocardial fibrosis.

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          Author and article information

          Journal
          CJNM
          Chinese Journal of Natural Medicines
          Elsevier
          1875-5364
          20 May 2018
          : 16
          : 5
          : 321-329
          Affiliations
          1Clinic Pharmacology Laboratory, Department of Pharmacy, The First Affiliated Hospital of Soochow University, Suzhou 215006, China
          2Department of Pharmacology, Jiangsu Key Laboratory of Preventive and Translational Medicine for Geriatric Diseases, College of Pharmaceutical Sciences, Soochow University, Suzhou 215123, China
          3Laboratory Department, Wuxi Center for Disease Control and Prevention, Wuxi 214023, China
          Author notes
          *Corresponding author: RONG Chen, E-mail: rongchen_76@ 123456aliyun.com

          ΔThese authors contributed equally to this work.

          These authors have no conflict of interest to declare.

          Article
          S1875-5364(18)30063-3
          10.1016/S1875-5364(18)30063-3
          29860992
          Copyright © 2018 China Pharmaceutical University. Published by Elsevier B.V. All rights reserved.
          Funding
          Funded by: National Nature Science Foundation of China
          Award ID: 81302772
          Funded by: Jiangsu Provincial Medical Talent Project
          Award ID: QNRC2016716
          This work was supported by the National Nature Science Foundation of China (No. 81302772), Jiangsu Provincial Medical Talent Project (No. QNRC2016716)

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