Cigarette smoke extract-induced adipogenesis in Graves' orbital fibroblasts is inhibited by quercetin via reduction in oxidative stress

Jin Sook Yoon, Hyun Jung Lee, Min Kyung Chae, Sang Yeul Lee, Eun Jig Lee

Research output: Contribution to journalArticle

26 Citations (Scopus)

Abstract

Cigarette smoking is known to aggravate Graves' orbitopathy (GO) severity by enhancing adipogenesis. We investigated the effect of quercetin, an antioxidant, on adipocyte differentiation induced by cigarette smoke extract (CSE) in primary cultured orbital fibroblasts (OFs) from GO patients. Freshly prepared CSE was added to the cells and H2O2 was used as a positive control. Intracellular reactive oxygen species (ROS) generation and adipogenesis were measured. The expressions of proteins peroxisome proliferator-activated receptor (PPAR) γ, CCAAT-enhancer-binding proteins (C/EBP) α and β, and heme oxygenase-1 (HO-1), an antioxidant enzyme, were examined during adipogenic differentiation. In result, CSE and H2O2 dose-dependently stimulated intracellular ROS production in normal and Graves' OFs. The effect of2%CSE was similar to that of 10 (μMH2O2; both concentrations were noncytotoxic and were used throughout the experiment. Quercetin pretreatment reduced the ROS generation stimulated by either CSE or H2O2 in preadipocyte OFs. CSE and H2O2 stimulated adipocyte differentiation in cultured OFs. The addition of quercetin (50 or 100mM) suppressed adipogenesis. Quercetin also suppressed ROS generation in differentiating OFs during adipogenesis stimulated by CSE and H2O2. Additionally, the expressions of PPARγ, C/EBPα, and C/EBPβ proteins were reduced in the quercetin-treated OFs. Quercetin also reduced the CSE- and H2O2-induced upregulation of ROS and HO-1 protein in differentiated OFs and preadipocyte OFs. As shown in this study, quercetin inhibited adipogenesis by reducing ROS in vitro, supporting the use of quercetin in the treatment of GO.

Original languageEnglish
Pages (from-to)145-156
Number of pages12
JournalJournal of Endocrinology
Volume216
Issue number2
DOIs
Publication statusPublished - 2013 Mar 21

Fingerprint

Adipogenesis
Quercetin
Smoke
Tobacco Products
Oxidative Stress
Fibroblasts
Reactive Oxygen Species
CCAAT-Enhancer-Binding Proteins
Peroxisome Proliferator-Activated Receptors
Heme Oxygenase-1
Adipocytes
Antioxidants
Proteins
Up-Regulation
Smoking
Enzymes

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cite this

@article{04e666f4438d43cd8dbda693c90d2455,
title = "Cigarette smoke extract-induced adipogenesis in Graves' orbital fibroblasts is inhibited by quercetin via reduction in oxidative stress",
abstract = "Cigarette smoking is known to aggravate Graves' orbitopathy (GO) severity by enhancing adipogenesis. We investigated the effect of quercetin, an antioxidant, on adipocyte differentiation induced by cigarette smoke extract (CSE) in primary cultured orbital fibroblasts (OFs) from GO patients. Freshly prepared CSE was added to the cells and H2O2 was used as a positive control. Intracellular reactive oxygen species (ROS) generation and adipogenesis were measured. The expressions of proteins peroxisome proliferator-activated receptor (PPAR) γ, CCAAT-enhancer-binding proteins (C/EBP) α and β, and heme oxygenase-1 (HO-1), an antioxidant enzyme, were examined during adipogenic differentiation. In result, CSE and H2O2 dose-dependently stimulated intracellular ROS production in normal and Graves' OFs. The effect of2{\%}CSE was similar to that of 10 (μMH2O2; both concentrations were noncytotoxic and were used throughout the experiment. Quercetin pretreatment reduced the ROS generation stimulated by either CSE or H2O2 in preadipocyte OFs. CSE and H2O2 stimulated adipocyte differentiation in cultured OFs. The addition of quercetin (50 or 100mM) suppressed adipogenesis. Quercetin also suppressed ROS generation in differentiating OFs during adipogenesis stimulated by CSE and H2O2. Additionally, the expressions of PPARγ, C/EBPα, and C/EBPβ proteins were reduced in the quercetin-treated OFs. Quercetin also reduced the CSE- and H2O2-induced upregulation of ROS and HO-1 protein in differentiated OFs and preadipocyte OFs. As shown in this study, quercetin inhibited adipogenesis by reducing ROS in vitro, supporting the use of quercetin in the treatment of GO.",
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Cigarette smoke extract-induced adipogenesis in Graves' orbital fibroblasts is inhibited by quercetin via reduction in oxidative stress. / Yoon, Jin Sook; Lee, Hyun Jung; Chae, Min Kyung; Lee, Sang Yeul; Lee, Eun Jig.

In: Journal of Endocrinology, Vol. 216, No. 2, 21.03.2013, p. 145-156.

Research output: Contribution to journalArticle

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T1 - Cigarette smoke extract-induced adipogenesis in Graves' orbital fibroblasts is inhibited by quercetin via reduction in oxidative stress

AU - Yoon, Jin Sook

AU - Lee, Hyun Jung

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N2 - Cigarette smoking is known to aggravate Graves' orbitopathy (GO) severity by enhancing adipogenesis. We investigated the effect of quercetin, an antioxidant, on adipocyte differentiation induced by cigarette smoke extract (CSE) in primary cultured orbital fibroblasts (OFs) from GO patients. Freshly prepared CSE was added to the cells and H2O2 was used as a positive control. Intracellular reactive oxygen species (ROS) generation and adipogenesis were measured. The expressions of proteins peroxisome proliferator-activated receptor (PPAR) γ, CCAAT-enhancer-binding proteins (C/EBP) α and β, and heme oxygenase-1 (HO-1), an antioxidant enzyme, were examined during adipogenic differentiation. In result, CSE and H2O2 dose-dependently stimulated intracellular ROS production in normal and Graves' OFs. The effect of2%CSE was similar to that of 10 (μMH2O2; both concentrations were noncytotoxic and were used throughout the experiment. Quercetin pretreatment reduced the ROS generation stimulated by either CSE or H2O2 in preadipocyte OFs. CSE and H2O2 stimulated adipocyte differentiation in cultured OFs. The addition of quercetin (50 or 100mM) suppressed adipogenesis. Quercetin also suppressed ROS generation in differentiating OFs during adipogenesis stimulated by CSE and H2O2. Additionally, the expressions of PPARγ, C/EBPα, and C/EBPβ proteins were reduced in the quercetin-treated OFs. Quercetin also reduced the CSE- and H2O2-induced upregulation of ROS and HO-1 protein in differentiated OFs and preadipocyte OFs. As shown in this study, quercetin inhibited adipogenesis by reducing ROS in vitro, supporting the use of quercetin in the treatment of GO.

AB - Cigarette smoking is known to aggravate Graves' orbitopathy (GO) severity by enhancing adipogenesis. We investigated the effect of quercetin, an antioxidant, on adipocyte differentiation induced by cigarette smoke extract (CSE) in primary cultured orbital fibroblasts (OFs) from GO patients. Freshly prepared CSE was added to the cells and H2O2 was used as a positive control. Intracellular reactive oxygen species (ROS) generation and adipogenesis were measured. The expressions of proteins peroxisome proliferator-activated receptor (PPAR) γ, CCAAT-enhancer-binding proteins (C/EBP) α and β, and heme oxygenase-1 (HO-1), an antioxidant enzyme, were examined during adipogenic differentiation. In result, CSE and H2O2 dose-dependently stimulated intracellular ROS production in normal and Graves' OFs. The effect of2%CSE was similar to that of 10 (μMH2O2; both concentrations were noncytotoxic and were used throughout the experiment. Quercetin pretreatment reduced the ROS generation stimulated by either CSE or H2O2 in preadipocyte OFs. CSE and H2O2 stimulated adipocyte differentiation in cultured OFs. The addition of quercetin (50 or 100mM) suppressed adipogenesis. Quercetin also suppressed ROS generation in differentiating OFs during adipogenesis stimulated by CSE and H2O2. Additionally, the expressions of PPARγ, C/EBPα, and C/EBPβ proteins were reduced in the quercetin-treated OFs. Quercetin also reduced the CSE- and H2O2-induced upregulation of ROS and HO-1 protein in differentiated OFs and preadipocyte OFs. As shown in this study, quercetin inhibited adipogenesis by reducing ROS in vitro, supporting the use of quercetin in the treatment of GO.

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