ABSTRACT
OBJECTIVE To study the protective effects of lycopene on cerebral vessels and neurons in hyperlipidemic model rats. METHODS SD rats were fed with hypercholesterolemia diet and ig administered with lycopene 5, 25, 45, 65, 85, 105 and 125 mg-kg-1 simultaneously every day for four weeks. At the same time, normal control group, hyperlipidemic model group and fluvastatin sodium (10 mg-kg-1) group were set up. Total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), oxidized low density lipoprotein (Ox-LDL), total antioxidant capacity (T-AOC), interleukin-1 (IL-1), tumor necrosis factor-a (TNF-α), vascular cell adhesion molecule-1 (VCAM-1), vascular endothelial growth factor (VEGF) and nitric oxide (NO) levels of the serum and brain were detected by kits. Claudin-5 glial fibrillary acidic protein (GFAP), phosphorylation-P38 protein (p-P38) levels in the brain were detected by Western blotting. Morphological changes of neurons were observed and counted by Nissl staining while lycopene levels were detected by high performance liquid chromatography. RESULTS Compared with the hyperlipidemic model group, serum and cerebral TC, TG, LDL-C, Ox-LDL, IL-1, TNF-a, VCAM-1, VEGF as well as cerebral NO, GFAP, p-P38 levels were decreased in lycopene (25-85 mg·kg-1) groups (PO.01), but serum T-AOC, NO and cerebral claudin-5 levels as well as the number of neurons were increased (PO.01). Serum TC, TG, LDL-C, IL-1, TNF-a and cerebral IL-1, TNF-a levels were decreased in lycopene 105 and 125 mg-kg"1 groups (P< 0.05), but serum NO levels were increased (P<0.01). The concentration of serum lycopene was quadratic with the dose of lycopene (P<0.01), and the concentrations of lycopene 65 and 85 mg·kg-1 groups were higher than those of other groups (P<0.01). CONCLUSION Lycopene cna reduce Ox-LDL formation mainly by affecting cholesterol levels in the blood, which alleviates the inflammatory response and maintains blood-brain barrier permeability. Activation in astrocytes is indirectly attenuated, and the production of p-P38 protein, IL-1, TNF-a and NO in the brain is decreased, which reduces hyperlipidemia-induced injury to cerebral vessels and neurons.