Aim To explore the mechanism of curcumin trinicotinate (CurTn) regulating vascular contractility and its effect on phenotype regulation of vascular smooth muscle cell (VSMC). Methods C57BL/6 mice were intragastrically administered with 50 mg/(kg·d) CurTn for 6 weeks. The thoracic aorta of the mice was taken after 6 weeks of continuous administration. The contractility of thoracic aorta was examined by tissue myograph system, and the levels of contractile proteins were detected in vascular tissues. VSMCs were treated with 10 μmol/L CurTn for 24 h; Western blot was used to detect the expressions of phenotypic related factors; The proliferation and migration of VSMC were observed by methyl thiazolyl tetrazolium staining and scratch assay; Oil red O staining and high performance liquid chromatography were used to analyze the phagocytosis of low density lipoprotein (LDL) by VSMC. Results The contractility of thoracic aorta vessel was enhanced and the expression of contractile protein in vascular smooth muscle tissue was increased in curTn-treated mice. Our results also showed that CurTn increased the expressions of myocardin and contractile-specific marker proteins α-actin and SM22α in VSMC, and decreased the level of osteopontin, a proliferative-specific marker. Further study found that the migration and proliferation of VSMC were inhibited by CurTn. LDL-treated VSMC was used to detect the effects of CurTn on lipid uptake, and it found that CurTn inhibited the phagocytosis of VSMC. Conclusion CurTn enhances vascular contractility, probably by promoting the contractile phenotype of VSMC and preventing its proliferative phenotype.