Abstract: AIM: To study the effects of cholestan-3β, 5α, 6β-triol (Triol ) and 25-hydroxycholesterol (25OH) on proliferation, apoptosis of vascular smooth muscle cells(VSMC) and to explore the effects and signifi-cance of oxysterols in atherogenesis.METHODS: VSMC of aorta of New Zealand white rabbit were cultured and i-dentified.VSMC incubated with or without Triol and 25OH or cholesterol, at different concentrations, was as experimental groups or control group.Cell proliferation was measured with WST-1.Cell apoptosis was evaluated by light and electron transmissionmicroscopy and terminal deoxynuocleotidyl transferase (TdT)-mediated dUPT nick-end labeling (TUNEL). RESULTS: The metabolic ac-tivity of VSMC wasnot different between at low dose (1× 10^-9 -1 ×10^-7 mol^·L^-1 ) of Triol and 25OH experi-mental groups and control group (P >0.05), but it de-creased significantly at higher dose (≥ 1 × 10^-6 mol^·L^-1 ) of oxysterols groups (P <0.01). After being treated with higher dose(≥20×10^-6 mol^·L^-1 ) of oxyterols, VSMC showed apoptosis of ultrastracture change including shrinkage, condensation of nuclear chro-matin, fragmentation nuclei and formation of apoptotic body.TUNEL revealed that Triol-induced apoptosis in VSMC was in a concentration-dependent manner.CONCLUSIONS: Triol and 25OH, at low dose, have not growth effect on VSMC, but at higher dose can induce VSMC apoptosis.Oxysterol-induced VSMC apoptosis may trigger plaque rupture and play an important role in atherogenesis.

Key words: oxysterol, vascular smooth muscle cell, proliferation, apoptosis, atherosclerosis