PMID- 12934384
OWN - NLM
STAT- MEDLINE
DCOM- 20040722
LR  - 20131121
IS  - 1000-5625 (Print)
IS  - 1000-5625 (Linking)
VI  - 28
IP  - 1
DP  - 2003 Feb 28
TI  - [Effect of triamcinolone acetonide on the proliferation and monocyte 
      chemoattractant protein expression in rat glomerular mesangial cells].
PG  - 13-6
AB  - OBJECTIVE: To explore the inhibitory effect and mechanism of triamcinolone 
      acetonide (TA) on the proliferation and monocyte chemoattractant protein-1(MCP-1) 
      expression in rat glomerular mesangial cells (GMCs). METHODS: TA with different 
      concentrations was put in the cultured rat GMC line in vitro after 
      Lipopolysaccharide (LPS). There were three groups in our experiment: the GMC 
      group, LPS group (GMCs + LPS), and TA group(GMCs + LPS + TA). The GMC 
      proliferation level was detected by the 
      3-(4,5-Dimethylthiazol-2-yl)2,5-diphenyltetrazo-lium bromid (MTT) incorporation 
      at the 24th and 48th hours. The expression of MCP-1 and nuclear transcriptional 
      factor-Kappa B (NF-kappa B) were checked by immunohistochemistry. The MCP-1 
      concentration was determined by ELISA. RESULTS: 1. In the TA group, the GMC 
      proliferative level was obviously lower than that either in the LPS group or in 
      the GMC group (P < 0.01). 2. The MCP-1 expression of GMCs in the TA group was 
      obviously lower than that in any of the other groups (P < 0.01). 3. The NF-kappa 
      B expression in GMCs in the TA group was significantly lower than that in the LPS 
      group (P < 0.01), but there was no significant difference in the NF-kappa B 
      expression between the TA group and LPS group (P > 0.05). 4. The concentration of 
      MCP-1 in the TA group was obviously lower than that in the LPS group (P < 0.01), 
      while there was no significant difference in the MCP-1 concentration between the 
      TA group and the GMC group (P > 0.05). CONCLUSION: TA can obviously inhibit the 
      proliferation of GMCs, and down-regulate the abnormal expression and secretion of 
      MCP-1 by reducing the activation of NF-kappa B.
FAU - Wu, Xiao-chuan
AU  - Wu XC
AD  - Laboratory of Pediatric Nephrology, Second Xiangya Hospital, Central South 
      University, Changsha 410011, China.
FAU - Yi, Zhu-wen
AU  - Yi ZW
FAU - Xiao, Jian-wu
AU  - Xiao JW
LA  - chi
PT  - English Abstract
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Hunan Yi Ke Da Xue Xue Bao
JT  - Hunan yi ke da xue xue bao = Hunan yike daxue xuebao = Bulletin of Hunan Medical 
      University
JID - 9424769
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glucocorticoids)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - F446C597KA (Triamcinolone Acetonide)
SB  - IM
MH  - Animals
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Down-Regulation
MH  - Glomerular Mesangium/cytology/*metabolism
MH  - Glucocorticoids/pharmacology
MH  - Lipopolysaccharides
MH  - NF-kappa B/biosynthesis/genetics
MH  - Rats
MH  - Triamcinolone Acetonide/*pharmacology
EDAT- 2003/08/26 05:00
MHDA- 2004/07/23 05:00
CRDT- 2003/08/26 05:00
PHST- 2003/08/26 05:00 [pubmed]
PHST- 2004/07/23 05:00 [medline]
PHST- 2003/08/26 05:00 [entrez]
PST - ppublish
SO  - Hunan Yi Ke Da Xue Xue Bao. 2003 Feb 28;28(1):13-6.