To evaluate the hepatoprotective effect of lycopene (Ly) on non-alcoholic fatty liver disease (NAFLD) in rat. A rat model of NAFLD was first established by feeding a high-fat diet for 14 wk. Sixty-five rats were randomly divided into normal group, model group and Ly treatment groups. Alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglycerides (TG), total cholesterol (TC) in serum and low density lipoprotein-cholesterol (LDL-C), high density lipoprotein-cholesterol (HDL-C), free fatty acid (FFA), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione (GSH) in liver tissue were evaluated, respectively. While the hepatoprotective effect was also confirmed by histopathological analysis, the expression levels of TNF-α and cytochrome P₄₅₀ (CYP) 2E1 in rat liver were determined by immunohistochemistry analysis. A significant decrease was observed in the levels of serum AST (2.07-fold), ALT (2.95-fold), and the blood lipid TG (2.34-fold) and TC (1.66-fold) in the dose of 20 mg/kg Ly-treated rats (P < 0.01), compared to the model group. Pretreatment with 5, 10 and 20 mg/kg of Ly significantly raised the levels of antioxidant enzyme SOD in a dose-dependent manner, to 90.95 ± 9.56, 109.52 ± 11.34 and 121.25 ± 10.68 (P < 0.05, P < 0.01), as compared with the model group. Similarly, the levels of GSH were significantly increased (P < 0.05, P < 0.01) after the Ly treatment. Meanwhile, pretreatment with 5, 10 and 20 mg/kg of Ly significantly reduced MDA amount by 30.87, 45.51 and 54.49% in the liver homogenates, respectively (P < 0.01). The Ly treatment group showed significantly decreased levels of lipid products LDL-C (P < 0.05, P < 0.01), improved HDL-C level and significantly decreased content of FFA, compared to the model group (P < 0.05, P < 0.01). Furthermore, the Ly-treated group also exhibited a down-regulated TNF-α and CYP2E1 expression, decreased infiltration of liver fats and reversed histopathological changes, all in a dose-dependent manner (P < 0.05, P < 0.01). This study suggests that Ly has a protective effect on NAFLD, down-regulates expression of TNF-α, and that CYP2E1 may be one of the action mechanisms for Ly.

Aim. Trimethylamine N-oxide (TMAO) has been demonstrated as an independent risk factor for cardiovascular disease. Our objective was to determine the plasma levels of TMAO in Chinese coronary heart disease (CHD) patients with or without type 2 diabetes mellitus (T2DM). Methods. A total of 132 control participants, 243 CHD patients, and 175 CHD patients with T2DM were enrolled. Plasma levels of TMAO in all patients were measured and analyzed. Results. The plasma levels of TMAO were significantly higher in CHD patients than in control subjects (3.08 ± 0.13 μM versus 1.49 ± 0.05 μM; P<0.01). In addition, plasma levels of TMAO were remarkably increased in CHD patients with T2DM compared with CHD patients (7.63 ± 0.97 μM versus 3.08 ± 0.13 μM; P<0.01). The receiver operating characteristic analysis revealed that the area under the curve of TMAO was 0.794 and 0.927 to predict CHD or CHD-T2DM patients (P<0.01). Univariate and multivariate logistic regression analysis showed that TMAO was an independent predictor in CHD patients with or without T2DM. The level of TMAO was correlated with high-sensitive troponin I (hs-TnI) and creatine kinase MB (CKMB). Conclusions. TMAO was an independent predictor of CHD in Chinese patients; moreover, the TMAO levels were highly associated with diabetes in CHD patients.