β-Carotene Inhibits Activation of NF-κB, Activator Protein-1, and STAT3 and Regulates Abnormal Expression of Some Adipokines in 3T3-L1 Adipocytes
10.15430/JCP.2018.23.1.37
- Author:
Soon Ok CHO
1
;
Min Hyun KIM
;
Hyeyoung KIM
Author Information
1. Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Adipocytes;
Adipokines;
Beta carotene;
Oxidative stress
- MeSH:
Adipocytes;
Adipokines;
Adiponectin;
Adipose Tissue, White;
Antioxidants;
beta Carotene;
Chemokine CCL2;
Chemokine CCL5;
DNA;
Electrophoretic Mobility Shift Assay;
Enzyme-Linked Immunosorbent Assay;
Inflammation;
Oxidative Stress;
Oxidoreductases;
Reactive Oxygen Species;
Real-Time Polymerase Chain Reaction;
RNA, Messenger;
Transcription Factor AP-1;
Transcription Factors
- From:Journal of Cancer Prevention
2018;23(1):37-43
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGROUND: Oxidative stress occurs in white adipose tissue and dysregulates the expression of adipokines secreted from adipocytes. Since adipokines influence inflammation, supplementation with antioxidants might be beneficial for preventing oxidative stress-mediated inflammation in adipocytes and inflammation-associated complications. β-Carotene is the most prominent antioxidant carotenoid and scavenges reactive oxygen species in various tissues. The purpose of this study was to determine whether β-carotene regulates the expression of adipokines, such as adiponectin, monocyte chemoattractant protein-1 (MCP-1), and regulated on activation, normal T cell expressed and secreted (RANTES) in 3T3-L1 adipocytes treated with glucose/glucose oxidase (G/GO). METHODS: 3T3-L1 adipocytes were cultured with or without β-carotene and treated with G/GO, which produces H2O2. mRNA and protein levels in the medium were determined by a real-time PCR and an ELISA. DNA binding activities of transcription factors were assessed using an electrophoretic mobility shift assay. RESULTS: G/GO treatment increased DNA binding affinities of redox-sensitive transcription factors, such as NF-κB, activator protein-1 (AP-1), and STAT3. G/GO treatment reduced the expression of adiponectin and increased the expression of MCP-1 and RANTES. G/GO-induced activations of NF-κB, AP-1, and STAT3 were inhibited by β-carotene. G/GO-induced dysregulation of adiponectin, MCP-1, and RANTES were significantly recovered by treatment with β-carotene. CONCLUSIONS: β-Carotene inhibits oxidative stress-induced inflammation by suppressing pro-inflammatory adipokines MCP-1 and RANTES, and by enhancing adiponectin in adipocytes. β-Carotene may be beneficial for preventing oxidative stress-mediated inflammation, which is related to adipokine dysfunction.
