PMID- 30651882
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20200930
IS  - 1792-0981 (Print)
IS  - 1792-1015 (Electronic)
IS  - 1792-0981 (Linking)
VI  - 17
IP  - 1
DP  - 2019 Jan
TI  - Thalidomide decreases high glucose-induced extracellular matrix protein synthesis 
      in mesangial cells via the AMPK pathway.
PG  - 927-934
LID - 10.3892/etm.2018.6995 [doi]
AB  - A previous study demonstrated the renal-protective effect of thalidomide (Thd) in 
      diabetic nephropathy rats through the activation of the adenosine 
      monophosphate-activated protein kinase (AMPK) and inhibition of the nuclear 
      factor kappaB (NF-kappaB)/monocyte chemoattractant protein-1 (MCP-1) and transforming 
      growth factor (TGF)-beta1/mothers against decapentaplegic homolog signaling 
      pathways. The association between AMPK inactivation and high glucose (HG)-induced 
      meningeal cell (MC) proliferation and extracellular matrix (ECM) accumulation via 
      NF-kappaB and TGF-beta1 signaling remains unknown. The aim of the current study was to 
      demonstrate the effects of Thd on cell proliferation and ECM expression in 
      HG-cultured MCs and the underlying mechanisms. HG-cultured human MCs were treated 
      with Thd. Cell proliferation was measured by MTT assay and quantification of cell 
      proliferation was based on the measurement of bromodeoxyuridine incorporation. 
      The differences in TGF-beta1, fibronectin and MCP-1 protein expression levels were 
      detected via ELISA and western blot analysis. The AMPK signaling pathway was also 
      examined by western blot analysis in MCs. Compound C, an AMPK inhibitor and AICAR 
      (5-aminoimidazole-4-carboxamide 1beta-D-ribofuranoside), an AMPK agonist, were used 
      to analyze the functional role of AMPK in MCs. Cell proliferation was 
      significantly decreased in HG-cultured MCs following treatment with high 
      concentrations of Thd (100 and 200 microg/ml) for 24 h compared with the HG-cultured 
      MC group. Thd suppressed the inflammatory processes in HG-induced MCs. These 
      effects were partially mediated through the activation of AMPK and inhibition of 
      the NF-kappaB/MCP-1 signaling pathways. Taken together, these results suggest that 
      Thd may have therapeutic potential in diabetic renal injury via the AMPK 
      signaling pathway.
FAU - Zhang, Hong-Xia
AU  - Zhang HX
AD  - Department of Nephrology, The Affiliated People's Hospital of Shanxi Medical 
      University, Shanxi Provincial People's Hospital, Taiyuan, Shanxi 030012, P.R. 
      China.
FAU - Yuan, Jie
AU  - Yuan J
AD  - Department of Radiology, The Affiliated People's Hospital of Shanxi Medical 
      University, Shanxi Provincial People's Hospital, Taiyuan, Shanxi 030012, P.R. 
      China.
FAU - Li, Ya-Feng
AU  - Li YF
AD  - Department of Nephrology, The Affiliated People's Hospital of Shanxi Medical 
      University, Shanxi Provincial People's Hospital, Taiyuan, Shanxi 030012, P.R. 
      China.
FAU - Li, Rong-Shan
AU  - Li RS
AD  - Department of Nephrology, The Affiliated People's Hospital of Shanxi Medical 
      University, Shanxi Provincial People's Hospital, Taiyuan, Shanxi 030012, P.R. 
      China.
LA  - eng
PT  - Journal Article
DEP - 20181120
PL  - Greece
TA  - Exp Ther Med
JT  - Experimental and therapeutic medicine
JID - 101531947
PMC - PMC6307482
OTO - NOTNLM
OT  - adenosine monophosphate-activated protein kinase
OT  - cell proliferation
OT  - diabetic nephropathy
OT  - nuclear factor kappaB
OT  - thalidomide
EDAT- 2019/01/18 06:00
MHDA- 2019/01/18 06:01
PMCR- 2018/11/20
CRDT- 2019/01/18 06:00
PHST- 2018/05/04 00:00 [received]
PHST- 2018/10/26 00:00 [accepted]
PHST- 2019/01/18 06:00 [entrez]
PHST- 2019/01/18 06:00 [pubmed]
PHST- 2019/01/18 06:01 [medline]
PHST- 2018/11/20 00:00 [pmc-release]
AID - ETM-0-0-6995 [pii]
AID - 10.3892/etm.2018.6995 [doi]
PST - ppublish
SO  - Exp Ther Med. 2019 Jan;17(1):927-934. doi: 10.3892/etm.2018.6995. Epub 2018 Nov 
      20.