Abstract: Objective The aim of this experiment was to explore the effect of panax notoginsenosides (PNS) on liver steatosis and nitric oxide (NO)-induced nitrogen monoxide synthase (iNOS)-nuclear factor kappa-B (NF-κB) pathway protein expression in mice with high-fat-induced non-alcoholic fatty liver diseases(NAFLD). Methods 40 male BALB/c mice were randomly divided into normal, model, PNS-intervened and simvastatin-intervened group, with 10 mice in each group. The NAFLD model in mice was established by feeding high fat diet for 12 weeks. After the successful model completion, the mice were feed with normal saline, PNS solution or simvastatin solution for 12 weeks. Serum total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were detected. The protein expressions of NO-iNOS-NF-κB pathway in liver tissues were detected by Western bloting. Results The body mass, liver mass and visceral fat ratio in PNS-intervened group were (31.6±1.7) g, (6.3±0.9) g and (3.4±0.5)%, significantly lower than [(36.5±2.0) g, (8.1±1.2) g and (4.3±0.8)%, P<0.05] in the model group; serum TC, TG and LDL-C levels were (2.5±0.8) mmol/L, (0.9±0.3) mmol/L and (1.1±0.3) mmol/L, significantly lower than [(4.5±1.6) mmol/L, (2.7±1.1) mmol/L and (2.3±0.6) mmol/L, respectively, P<0.05], while serum HDL-C level was (0.4±0.2) mmol/L, significantly higher than (0.2±0.1) mmol/L in the model group (P<0.05); serum ALT and AST levels were (32.5±6.8)U/L and (41.3±6.8)U/L, significantly lower than [(65.2±8.7)U/L and (62.7±6.9)U/L, respectively, P<0.05] in the model group; the relative protein expressions of NO, iNOS and p-NF-κB were (1.2±0.2), (1.1±0.1) and (1.2±0.2), significantly lower than [(5.3±0.6), (4.8±0.5) and (5.6±0.5), respectively, P<0.05] in the model group. Conclusion PNS could effectively reduce blood lipids levels and alleviate liver steatosis in mice with NAFLD, which might be related to the inhibition NO/iNOS/NF-κB pathway protein expression.

Key words: Non-alcoholic fatty liver disease, Panax notoginsenosides, Liver steatosis, Nitric oxide -induced nitrogen monoxide synthase -nuclear factor kappa-B pathway, Mice