PMID- 25738264
OWN - NLM
STAT- MEDLINE
DCOM- 20160115
LR  - 20180815
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 12
IP  - 1
DP  - 2015 Jul
TI  - Testosterone enhances lipopolysaccharide-induced interleukin-6 and macrophage 
      chemotactic protein-1 expression by activating the extracellular signal-regulated 
      kinase 1/2/nuclear factor-kappaB signalling pathways in 3T3-L1 adipocytes.
PG  - 696-704
LID - 10.3892/mmr.2015.3401 [doi]
AB  - Low-grade chronic inflammation is commonly found in patients with polycystic 
      ovary syndrome (PCOS) who exhibit hyperandrogenism or hyperandrogenemia. Clinical 
      studies have shown that hyperandrogenemia is closely correlated with low-grade 
      chronic inflammation. However, the mechanism underlying this correlation remains 
      unclear. Recent studies have suggested that adipocytes increase the production of 
      proinflammatory mediators such as interleukin-6 (IL-6) and macrophage chemotactic 
      protein-1 (MCP-1) when the inflammatory signal transduction cascade system is 
      activated by external stimuli. The present study aimed to evaluate the effects of 
      testosterone on the innate signalling and expression of proinflammatory mediators 
      in 3T3-L1 adipocytes, which were or were not induced by lipopolysaccharide (LPS). 
      The effects of testosterone on the expression of proinflammatory mediators, 
      nuclear factor-kappaB (NF-kappaB), and extracellular signal-regulated kinase 1/2 (ERK1/2) 
      signalling pathways were investigated using an enzyme-linked immunosorbent assay, 
      reverse transcriptase-polymerase chain reaction, western blot analysis and an 
      electrophoresis mobility shift assay. Testosterone induces IL-6 and MCP-1, and 
      enhances LPS-induction of IL-6 and MCP-1. However, the effects are not simply 
      additive, testosterone significantly enhanced the effects of LPS-induced 
      inflammation factors. Testosterone induces the phosphorylation of ERK1/2 and 
      NF-kappaB. The effect of testosterone on the expression of IL-6 and MCP-1 is 
      inhibited by PD98059 , an ERK1/2 inhibitor, and PDTC, an NF-kappaB inhibitor. The 
      results indicate that testosterone enhances LPS-induced IL-6 and MCP-1 expression 
      by activating the ERK1/2/NF-kappaB signalling pathways in 3T3-L1 adipocytes.
FAU - Su, Chunlin
AU  - Su C
AD  - Department of Gynecology, Shanghai Obstetrics and Gynecology Hospital Affiliated 
      to Fudan University, Shanghai 200011, P.R. China.
FAU - Chen, Min
AU  - Chen M
AD  - Department of Reproductive Medicine Center, Shuguang Hospital Affiliated to 
      Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
FAU - Huang, Haiyan
AU  - Huang H
AD  - Key Laboratory of Molecular Medicine Ministry of Education, Shanghai Medical 
      University Affliated to Fudan University, Shanghai 200011, P.R. China.
FAU - Lin, Jinfang
AU  - Lin J
AD  - Department of Gynecology, Shanghai Obstetrics and Gynecology Hospital Affiliated 
      to Fudan University, Shanghai 200011, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150303
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Ccl2 protein, mouse)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Flavonoids)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Thiocarbamates)
RN  - 135467-92-4 (prolinedithiocarbamate)
RN  - 3XMK78S47O (Testosterone)
RN  - 9DLQ4CIU6V (Proline)
RN  - SJE1IO5E3I (2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one)
SB  - IM
MH  - 3T3-L1 Cells
MH  - Adipocytes/drug effects/metabolism
MH  - Animals
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Female
MH  - Flavonoids/administration & dosage
MH  - Gene Expression Regulation/drug effects
MH  - Inflammation/chemically induced/*genetics/pathology
MH  - Interleukin-6/*biosynthesis/genetics
MH  - Lipopolysaccharides/toxicity
MH  - MAP Kinase Signaling System/drug effects
MH  - Mice
MH  - NF-kappa B/antagonists & inhibitors/genetics
MH  - Proline/administration & dosage/analogs & derivatives
MH  - Testosterone/*administration & dosage/metabolism
MH  - Thiocarbamates/administration & dosage
EDAT- 2015/03/05 06:00
MHDA- 2016/01/16 06:00
CRDT- 2015/03/05 06:00
PHST- 2014/02/28 00:00 [received]
PHST- 2014/12/02 00:00 [accepted]
PHST- 2015/03/05 06:00 [entrez]
PHST- 2015/03/05 06:00 [pubmed]
PHST- 2016/01/16 06:00 [medline]
AID - 10.3892/mmr.2015.3401 [doi]
PST - ppublish
SO  - Mol Med Rep. 2015 Jul;12(1):696-704. doi: 10.3892/mmr.2015.3401. Epub 2015 Mar 3.