Figure 1.

Nuciferine alleviates lipid accumulation, insulin resistance, oxidative stress and inflammatory response in the liver of high-fat diet (HFD) mice. Mice were fed either a normal diet (ND) or an HFD for 16 weeks. Nuciferine-treated mice were fed an HFD for 12 weeks and then fed an HFD containing low dose nuciferine (HFLN) or high dose nuciferine (HFHN) for another 4 weeks. (A) Chemical structure of nuciferine. (B–D) Body weight, liver weight and ratio of liver weight to body weight (LW/BW). (E) Gross anatomical views of representative mouse liver. Scale bar, 2 cm. (F) Representative images of H&E and Oil-red O staining of liver sections (original magnification 20 ×). (G, H) Hepatic and serum triglyceride contents. (I, J) Fasting blood glucose and insulin levels. (K) Homeostasis model assessment of insulin resistance index. (L, M) Glucose-tolerance test (GTT) and insulin-tolerance test (ITT). (N) Representative immunoblotting of insulin receptor (IR), phospho (p)-IR, protein kinase B (AKT) and p-AKT in the livers from different groups and quantification of p-IR/IR, p-AKT/AKT and expressed as fold change relative to ND group. (O, P) Hepatic malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) contents. (Q, R) Hepatic superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities. (S) Representative immunoblotting of nuclear factor kappa B (NF-κB), p-NF-κB and IκBα in the livers from different groups and quantification of p-NF-κB/NF-κB and IκBα/β-actin and expressed as fold change relative to ND group. All experiments were repeated at least 3 times. n = 9 mice per group for B–D, G–M and O–R; n = 6 mice per group for N and S. Data were expressed as the mean ± SEM; ∗P < 0.05, ∗∗P < 0.01.