Experimental study on effect of allicin in inhibiting insulin-induced vascular smooth muscle cell proliferation and migration.
- Author:
Ting LI
;
Yong XIA
- Publication Type:Journal Article
- MeSH: Animals; Cell Movement; drug effects; Cell Proliferation; drug effects; Cells, Cultured; Insulin; metabolism; Male; Muscle, Smooth, Vascular; cytology; drug effects; metabolism; Myocytes, Smooth Muscle; cytology; drug effects; Plant Extracts; pharmacology; Rats; Rats, Sprague-Dawley; Sulfinic Acids; pharmacology
- From: China Journal of Chinese Materia Medica 2014;39(20):4040-4044
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of allicin in inhibiting insulin-induced vascular smooth muscle cell (VSMC) proliferation and migration.
METHODThe tissue explant method was adopted to culture rat's aVSMCs, and the immunofluorescence method was used to identify α-SMA. Cells from the third to fifth generations were selected in the experiment The insulin-induced VSMC model was established. The experiment was carried out in five groups: the control group, the insulin group, the allicin group, the ERK inhibitors PD98059 group (20 μmol · L(-1)) and the PD98059 + allicin group. VSMCs' proliferation was determined by CCK8 colorimetric method, while its migration was detected by cell counting; The western blotting was used to detect total ERK, Phospho-ERK, PCNA protein's expression.
RESULTPrimary cultured VSMCs grew well in the spindle shape under the lightmicroscope, with peak and valley. α-SMA immunofluorescence results showed that the cultured cells had typical VSMCs' features. Insulin could stimulate VSMCs' proliferation and migration, with the best effect at the concentration of 100 nmol · L(-1). The pretreatment with allicin could significantly inhibit VSMCs' proliferation and migration induced by insulin in a dose-dependent manner. The pretreatment with PD98059 and allicin + PD98059 could inhibit VSMCs' proliferation and migration induced by insulin remarkably as well. Insulin could significantly accelerate VSMCs' expression of such proteins as p-ERK, PCNA. Contrarily, allicin could notably inhibit VSMCs' expression of such proteins as p-ERK, PCNA in a dose-dependent manner.
CONCLUSIONAllicin could significantly inhibit VSMCs' proliferation and migration induced by insulin, which may be related to the inhibition of the activation of ERK signal path.