〔Abstract〕 Objective To investigate the roles of miR-29 c in regulating the expression of silent mating type information regulation 2 homolog-1(SIRT1) involved in atherosclerosis(AS) oxidative stress and inflammatory processes. Methods After adaptive feeding, ApoE-/-knockout mice(ApoE-/-) were fed with a high-fat diet to build the atherosclerosis model at 6 weeks of age. In addition, C57 BL/6 J mice was used as the normal control group and fed with normal feed. After 12 weeks, the expression of miR-29 c, tumor necrosis factor-α(TNF-α) mRNA, reactive oxygen species(ROS) production and nicotinamide adenine dinucleotide phosphate(NADPH) oxidase activity were detected in mouse aorta. Meanwhile, human umbilical vein endothelial cells(HUVEC) were culturedin vitro, transfected with miR-29 c mimic and antagomir respectively and stimulated with oxidized low density lipoprotein(oxLDL)(50 μg/ml). The levels of TNF-α, ROS and NADPH oxidase activity were tested in each group. Besides, the expression of SIRT1 mRNA and protein were detected in HUVEC after the stimulation of oxLDL by real time PCR and Western blot, which were also determined in miR-29 c mimic and antagomir group. Results The results showed that the expression of miR-29 c, TNF-α mRNA, ROS and NADPH oxidase activity significantly increased in AS group compared with the normal group. Under the stimulation of oxLDL, compared with the control group, the levels of TNF-α, ROS and NADPH oxidase activity in the cells decreased significantly when treated with miR-29 c antagomir. On the contrary, the levels of TNF-α, ROS and NADPH oxidase activity were significantly increased after miR-29 c mimic treatment. In addition, the expression of SIRT1 mRNA and protein were reduced in HUVEC after the stimulation of oxLDL. However, compared with the control group, there was no statistical difference in SIRT1 mRNA level in the antagomir and mimic groups, but the expression of SIRT1 protein was significant difference in the antagomir and mimic groups. The above indicated that the modulation of SIRT1 induced by miR-29 c was at the post-translational level. Conclusion miR-29 c can down-regulate the expression of SIRT1 and enhance oxidative stress and inflammatory response in the process of AS.