Effect of S-adenosylmethionine on vascular smooth cells proliferation and migration.
- Author:
Cheng-ji JIN
1
;
Xiao-mei WANG
;
Wei DUAN
;
Xiang LI
;
Jian-mei QU
;
Tao ZHANG
;
Jing-yao LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Movement; drug effects; Cell Proliferation; drug effects; Cells, Cultured; Male; Muscle, Smooth, Vascular; cytology; metabolism; Myocytes, Smooth Muscle; drug effects; metabolism; NF-kappa B; metabolism; Platelet-Derived Growth Factor; genetics; Rats; Rats, Sprague-Dawley; S-Adenosylmethionine; pharmacology; Tumor Necrosis Factor-alpha; pharmacology; Tunica Intima; drug effects
- From: Chinese Journal of Cardiology 2012;40(10):869-873
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of S-adenosyl-L-methionine (SAMe) on vascular smooth muscle cells (VSMCs) proliferation and migration and neointima formation in rat carotid artery balloon injury model.
METHODSRat VSMCs were divided into control group, TNF-α (10 ng/ml) group, SAMe (0.2 mmol/L) group and TNF-α + SAMe group. VSMC migration distance and proliferation were examined by cell scrape tests and MTT method. NF-κB activity was analyzed by EMSA. PDGF mRNA expression was detected by Northern blot. SD rat were divided into control group, carotid balloon injury group treated with saline or SAMe (15 mg×kg(-1)×d(-1) for 14 d), then blood vessel proliferation was observed histologically in rat carotid artery.
RESULTS(1) In vitro, the VSMCs migration distance, absorbance at 490 nm, PDGF mRNA expression, NF-κB activity were all increased in TNF-α group compared to the control group (P < 0.01), and decreased in TNF-α + SAMe group compared to the TNF-α group (P < 0.01). (2) In the balloon injury in vivo models, the intima area of saline group and SAMe group was increased compared to the control group, while the lumen area was larger and the intima area was smaller in the SAMe group than in the saline group (all P < 0.05).
CONCLUSIONSAMe could reduce TNF-α induced VSMC proliferation and migration possibly through inhibiting NF-κB activity and downregulating PDGF gene expression.