Objective CD36 plays pivotal role in atherosclerosis development, beside lipid accumulation itself. CD36 that is expressed on membrane surface of macrophage will facilitate and assist macrophage in binding and uptake oxidized LDL (oxLDL) and promotes foam cell formation and plaque development. Chitosan, cationic polymer obtained by deacetylation of chitin, has been demonstrated to lower cholesterol level and inhibit plaque progression in animal models of atherosclerosis. This study aimed to analyze possible effect of chitosan on atherosclerosis through reduction of CD36 expression and its effects on intimal thickening. Methods Adult male Wistar rats were injected by epinephrine 0.006 mg once before intervention. Rats then were fed with high fat diet while receiving various concentrations of chitosan (5%, 10%, 25%, or 50%) or placebo for control group. After 30 days treatment, rats were sacrificed and abdominal aorta was taken. The expression of CD36 receptor was evaluated by immunohistochemistry staining using rabbit anti-CD36/PAS-4 polyclonal antibody and analyzed by software assisted morphometric analysis. Meanwhile, intimal thickness was measured using HE staining. Results The expression of CD36 on intima was significantly lowered in dose dependent manner upon chitosan treatment, compared to control group (P = 0,000). In parallel with the reduction of CD36, chitosan caused gradual decline of intimal thickness with the lowest intimal thickness mean was seen in 50% group (mean: 1,30 ± 8.82 nm). However, those findings were not statistically significant. Conclusion These findings supported therapeutic role of chitosan on atherosclerosis plaque formation through reduction of CD36 expression and decrease intimal thickening.