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Title: Scoparone attenuates RANKL-induced osteoclastic differentiation through controlling reactive oxygen species production and scavenging

Abstract

Scoparone, one of the bioactive components of Artemisia capillaris Thunb, has various biological properties including immunosuppressive, hepatoprotective, anti-allergic, anti-inflammatory, and antioxidant effects. This study aims at evaluating the anti-osteoporotic effect of scoparone and its underlying mechanism in vitro. Scoparone demonstrated potent cellular antioxidant capacity. It was also found that scoparone inhibited the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation and suppressed cathepsin K and tartrate-resistant acid phosphatase (TRAP) expression via c-jun N-terminal kinase (JNK)/extracellular signal-regulated kinase (ERK)/p38-mediated c-Fos–nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) signaling pathway. During osteoclast differentiation, the production of general reactive oxygen species (ROS) and superoxide anions was dose-dependently attenuated by scoparone. In addition, scoparone diminished NADPH (nicotinamide adenine dinucleotide phosphate) oxidase 1 (Nox1) expression and activation via the tumor necrosis factor receptor-associated factor 6 (TRAF6)–cSrc–phosphatidylinositol 3-kinase (PI3k) signaling pathway and prevented the disruption of mitochondrial electron transport chain system. Furthermore, scoparone augmented the expression of superoxide dismutase 1 (SOD1) and catalase (CAT). The overall results indicate that the inhibitory effect of scoparone on RANKL-induced osteoclast differentiation is attributed to the suppressive effect on ROS and superoxide anion production by inhibiting Nox1 expression and activation and protecting the mitochondrial electron transport chain systemmore » and the scavenging effect of ROS resulting from elevated SOD1 and CAT expression. - Highlights: • Scoparone dose-dependently inhibited RANKL-induced osteoclast differentiation. • Scoparone diminished general ROS and superoxide anions in a dose-dependent manner. • Scoparone inhibited Nox1 expression and activation. • Scoparone prevented the disruption of mitochondrial electron transport chain system. • Scoparone augmented superoxide dismutase and catalase expression.« less

Authors:
;
Publication Date:
OSTI Identifier:
22462260
Resource Type:
Journal Article
Resource Relation:
Journal Name: Experimental Cell Research; Journal Volume: 331; Journal Issue: 2; Other Information: Copyright (c) 2015 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA)
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; ACID PHOSPHATASE; ANIONS; ANTIOXIDANTS; CATALASE; CATHEPSINS; CATS; DOSES; ELECTRONS; GUANOSINE; LIGANDS; MITOCHONDRIA; NADP; OXIDASES; OXYGEN; PHOSPHORUS 38; RADIOPROTECTIVE SUBSTANCES; RECEPTORS; SIGNALS; SUPEROXIDE DISMUTASE

Citation Formats

Lee, Sang-Hyun, and Jang, Hae-Dong, E-mail: haedong@hnu.kr. Scoparone attenuates RANKL-induced osteoclastic differentiation through controlling reactive oxygen species production and scavenging. United States: N. p., 2015. Web. doi:10.1016/J.YEXCR.2014.12.018.
Lee, Sang-Hyun, & Jang, Hae-Dong, E-mail: haedong@hnu.kr. Scoparone attenuates RANKL-induced osteoclastic differentiation through controlling reactive oxygen species production and scavenging. United States. doi:10.1016/J.YEXCR.2014.12.018.
Lee, Sang-Hyun, and Jang, Hae-Dong, E-mail: haedong@hnu.kr. Sun . "Scoparone attenuates RANKL-induced osteoclastic differentiation through controlling reactive oxygen species production and scavenging". United States. doi:10.1016/J.YEXCR.2014.12.018.
@article{osti_22462260,
title = {Scoparone attenuates RANKL-induced osteoclastic differentiation through controlling reactive oxygen species production and scavenging},
author = {Lee, Sang-Hyun and Jang, Hae-Dong, E-mail: haedong@hnu.kr},
abstractNote = {Scoparone, one of the bioactive components of Artemisia capillaris Thunb, has various biological properties including immunosuppressive, hepatoprotective, anti-allergic, anti-inflammatory, and antioxidant effects. This study aims at evaluating the anti-osteoporotic effect of scoparone and its underlying mechanism in vitro. Scoparone demonstrated potent cellular antioxidant capacity. It was also found that scoparone inhibited the receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclast differentiation and suppressed cathepsin K and tartrate-resistant acid phosphatase (TRAP) expression via c-jun N-terminal kinase (JNK)/extracellular signal-regulated kinase (ERK)/p38-mediated c-Fos–nuclear factor of activated T cells, cytoplasmic 1 (NFATc1) signaling pathway. During osteoclast differentiation, the production of general reactive oxygen species (ROS) and superoxide anions was dose-dependently attenuated by scoparone. In addition, scoparone diminished NADPH (nicotinamide adenine dinucleotide phosphate) oxidase 1 (Nox1) expression and activation via the tumor necrosis factor receptor-associated factor 6 (TRAF6)–cSrc–phosphatidylinositol 3-kinase (PI3k) signaling pathway and prevented the disruption of mitochondrial electron transport chain system. Furthermore, scoparone augmented the expression of superoxide dismutase 1 (SOD1) and catalase (CAT). The overall results indicate that the inhibitory effect of scoparone on RANKL-induced osteoclast differentiation is attributed to the suppressive effect on ROS and superoxide anion production by inhibiting Nox1 expression and activation and protecting the mitochondrial electron transport chain system and the scavenging effect of ROS resulting from elevated SOD1 and CAT expression. - Highlights: • Scoparone dose-dependently inhibited RANKL-induced osteoclast differentiation. • Scoparone diminished general ROS and superoxide anions in a dose-dependent manner. • Scoparone inhibited Nox1 expression and activation. • Scoparone prevented the disruption of mitochondrial electron transport chain system. • Scoparone augmented superoxide dismutase and catalase expression.},
doi = {10.1016/J.YEXCR.2014.12.018},
journal = {Experimental Cell Research},
number = 2,
volume = 331,
place = {United States},
year = {Sun Feb 15 00:00:00 EST 2015},
month = {Sun Feb 15 00:00:00 EST 2015}
}