PMID- 27592629
OWN - NLM
STAT- MEDLINE
DCOM- 20170720
LR  - 20181113
IS  - 1880-3873 (Electronic)
IS  - 1340-3478 (Print)
IS  - 1340-3478 (Linking)
VI  - 24
IP  - 3
DP  - 2017 Mar 1
TI  - Whitmania Pigra Whitman Extracts Inhibit Lipopolysaccharide Induced Rat Vascular 
      Smooth Muscle Cells Migration and their Adhesion Ability to THP-1 and RAW 264.7 
      Cells.
PG  - 301-311
LID - 10.5551/jat.36558 [doi]
AB  - AIM: Atherosclerosis is a kind of chronic inflammatory disease. A crucial 
      pathology change of atherosclerosis is the migration of activated VSMCs to the 
      intima where they interact with leukocytes by expressing adhesion molecules, 
      including intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell 
      adhesion molecule-1 (VCAM-1). Moreover, monocyte chemoattractant protein-1 
      (MCP-1) expressed by VSMCs plays an important role in recruiting monocytes and 
      macrophages. Leech (Whitmania pigra Whitman) is a traditional Chinese medicine to 
      treat cardiovascular diseases including atherosclerosis, however previous 
      research has rarely reported the molecular mechanism for its curative effect. 
      Thus, our study focuses on the effects of leech extracts on the expression of 
      inflammatory factors, adhesion molecules and MCP-1 in rat VSMCs. METHODS: In our 
      present study, wound-healing assay and Boyden chamber model were applied to 
      evaluate the anti-migration effect of LEE (Leech Enzyme Extracts) on LPS induced 
      VSMCs. The anti-adhesion effect was assessed using DiI-labeled THP-1 and 
      RAW264.7. RESULTS: LEE suppressed LPS-induced VSMCs migration and decreased the 
      chemotaxis and adhesive capacity of THP-1 and RAW264.7 to LPS-stimulated VSMCs. 
      LEE also attenuated the upregulation of a variety of pro-atherosclerotic factors 
      by inhibiting the phosphorylation of p38 MAPK. LEE was also observed to prevent 
      NF-kappaB p65 nuclear localization using immune-fluorescent staining. CONCLUSIONS: In 
      conclusion, LEE suppresses LPS-induced upregulation of inflammatory factors, 
      adhesion molecules and MCP-1 in rat VSMCs mainly via inhibiting the p38 
      MAPK/NF-kappaB pathways, thus partly uncovered LEE's molecular mechanisms for its 
      therapeutic effect on atherosclerosis.
FAU - Li, Shuaishuai
AU  - Li S
AD  - Marine College, Shandong University.
FAU - Cheng, Long
AU  - Cheng L
FAU - An, Dengkun
AU  - An D
FAU - Song, Shuliang
AU  - Song S
FAU - Liang, Hao
AU  - Liang H
FAU - Chu, Fulong
AU  - Chu F
FAU - Ji, Aiguo
AU  - Ji A
LA  - eng
PT  - Journal Article
DEP - 20160902
PL  - Japan
TA  - J Atheroscler Thromb
JT  - Journal of atherosclerosis and thrombosis
JID - 9506298
RN  - 0 (Fibrinolytic Agents)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (RNA, Messenger)
SB  - IM
MH  - Animals
MH  - Blotting, Western
MH  - Cell Adhesion/*drug effects
MH  - Cell Movement/*drug effects
MH  - Cells, Cultured
MH  - Fibrinolytic Agents/*pharmacology
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Leeches/enzymology
MH  - Lipopolysaccharides
MH  - Macrophages/*drug effects/metabolism/pathology
MH  - Male
MH  - Mice
MH  - Monocytes/*drug effects/metabolism/pathology
MH  - Muscle, Smooth, Vascular/*drug effects/metabolism/pathology
MH  - Phosphorylation
MH  - RAW 264.7 Cells
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Real-Time Polymerase Chain Reaction
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction
PMC - PMC5383546
COIS- All authors approved the final submission and declare that no potential competing 
      interests exist.
EDAT- 2016/09/07 06:00
MHDA- 2017/07/21 06:00
PMCR- 2017/03/01
CRDT- 2016/09/06 06:00
PHST- 2016/09/07 06:00 [pubmed]
PHST- 2017/07/21 06:00 [medline]
PHST- 2016/09/06 06:00 [entrez]
PHST- 2017/03/01 00:00 [pmc-release]
AID - 10.5551/jat.36558 [doi]
PST - ppublish
SO  - J Atheroscler Thromb. 2017 Mar 1;24(3):301-311. doi: 10.5551/jat.36558. Epub 2016 
      Sep 2.