PMID- 29629347
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220316
IS  - 2288-3649 (Print)
IS  - 2288-3657 (Electronic)
IS  - 2288-3649 (Linking)
VI  - 23
IP  - 1
DP  - 2018 Mar
TI  - beta-Carotene Inhibits Activation of NF-kappaB, Activator Protein-1, and STAT3 and 
      Regulates Abnormal Expression of Some Adipokines in 3T3-L1 Adipocytes.
PG  - 37-43
LID - 10.15430/JCP.2018.23.1.37 [doi]
AB  - 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. beta-Carotene is the most prominent 
      antioxidant carotenoid and scavenges reactive oxygen species in various tissues. 
      The purpose of this study was to determine whether beta-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 beta-carotene and treated 
      with G/GO, which produces H(2)O(2). 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-kappaB, 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-kappaB, AP-1, and 
      STAT3 were inhibited by beta-carotene. G/GO-induced dysregulation of adiponectin, 
      MCP-1, and RANTES were significantly recovered by treatment with beta-carotene. 
      CONCLUSIONS: beta-Carotene inhibits oxidative stress-induced inflammation by 
      suppressing pro-inflammatory adipokines MCP-1 and RANTES, and by enhancing 
      adiponectin in adipocytes. beta-Carotene may be beneficial for preventing oxidative 
      stress-mediated inflammation, which is related to adipokine dysfunction.
FAU - Cho, Soon Ok
AU  - Cho SO
AD  - Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea.
FAU - Kim, Min-Hyun
AU  - Kim MH
AD  - Department of Molecular and Integrative Physiology, University of Michigan 
      Medical School, Ann Arbor, MI, USA.
FAU - Kim, Hyeyoung
AU  - Kim H
AD  - Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human 
      Ecology, Yonsei University, Seoul, Korea.
LA  - eng
PT  - Journal Article
DEP - 20180330
PL  - Korea (South)
TA  - J Cancer Prev
JT  - Journal of cancer prevention
JID - 101615965
PMC - PMC5886493
OTO - NOTNLM
OT  - Adipocytes
OT  - Adipokines
OT  - Beta carotene
OT  - Oxidative stress
COIS- CONFLICTS OF INTEREST No potential conflicts of interest were disclosed.
EDAT- 2018/04/10 06:00
MHDA- 2018/04/10 06:01
PMCR- 2018/03/01
CRDT- 2018/04/10 06:00
PHST- 2018/02/28 00:00 [received]
PHST- 2018/03/19 00:00 [revised]
PHST- 2018/03/19 00:00 [accepted]
PHST- 2018/04/10 06:00 [entrez]
PHST- 2018/04/10 06:00 [pubmed]
PHST- 2018/04/10 06:01 [medline]
PHST- 2018/03/01 00:00 [pmc-release]
AID - jcp-23-037 [pii]
AID - 10.15430/JCP.2018.23.1.37 [doi]
PST - ppublish
SO  - J Cancer Prev. 2018 Mar;23(1):37-43. doi: 10.15430/JCP.2018.23.1.37. Epub 2018 
      Mar 30.