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 language | English |
|---|---|
| Pages (from-to) | 145-156 |
| Number of pages | 12 |
| Journal | Journal of Endocrinology |
| Volume | 216 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2013 Mar 21 |
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All Science Journal Classification (ASJC) codes
- Endocrinology, Diabetes and Metabolism
- Endocrinology
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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 journal › Article
TY - JOUR
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
AU - Chae, Min Kyung
AU - Lee, Sang Yeul
AU - Lee, Eun Jig
PY - 2013/3/21
Y1 - 2013/3/21
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.
UR - http://www.scopus.com/inward/record.url?scp=84874762098&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84874762098&partnerID=8YFLogxK
U2 - 10.1530/JOE-12-0257
DO - 10.1530/JOE-12-0257
M3 - Article
C2 - 23143154
AN - SCOPUS:84874762098
VL - 216
SP - 145
EP - 156
JO - Journal of Endocrinology
JF - Journal of Endocrinology
SN - 0022-0795
IS - 2
ER -