Atorvastatin attenuates inflammatory infiltration and vascular remodeling in lung of hypercholesterolemia rabbits

Hypercholesterolemia contributes to cardiovascular diseases, but its direct effect on lung is little known. 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to exert numerous effects that are dependent and independent of their cholesterol-lowering property. The authors hypothesized that atorvastatin would attenuate hypercholesterolemia-induced lesion in lung. Fifteen rabbits were randomly divided into control group, high-cholesterol forage group, and atrovastatin treatment group. Body weight and blood lipid were measured. All lung tissue and pulmonary arteries were collected for histopathology and immunohistochemistry. Alveolar macrophages (AMs) were cultured and activation of nuclear factor (NF)-kappa B was detected. Concentrations of interleukin (IL)-6 were measured in serum, bronchoalveolar lavage fluid (BALF), and culture supernatants of AMs. Total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) of high-cholesterol forage group were higher than control group (P < .05). There were infiltrating of AMs and lymphocytes in lung tissue of high-cholesterol forage group. NF-kappa B activity in AMs and concentrations of IL-6 in serum, BALF, and culture supernatants of AMs were higher than those of control group (P < .01), and so were all vascular remodeling indexes. TC and LDL-C and other indexes of atrovastatin treatment group were decreased (P < .05). Hypercholesterolemia induced pulmonary inflammatory Infiltration and vascular remodeling. Atorvastatin attenuated inflammatory infiltration and vascular remodeling in lung of hypercholesterolemia rabbits.