Table 1.
Mouse primers for real-time polymerase chain reaction.
Table 2.
Effect of atorvastatin on serum parameters of ApoE-/- mice with or without casein injection.
Fig 1.
Effect of atorvastatin on lipid accumulation in livers of ApoE-/- mice.
Liver sections of representative mice from each group were stained with (A) H&E or (B) Oil Red O. The contents of liver (C) TC, (D) TG and (E) FFA were quantified as described in methods (n = 6). (F) The mRNA expressions of lipogenic genes in livers of ApoE-/- mice (n = 6). (G) The protein expressions of lipogenic genes in livers of ApoE-/- mice (n = 3). The histogram represents the densitometric scans for target protein bands normalized by β-actin and expressed as fold changes relative to protein expression in control mice. The results are depicted as mean ± SD, *P<0.05 versus control group, #P<0.05 versus casein injected alone group.
Fig 2.
Effect of atorvastatin on hepatic inflammatory injury in ApoE-/- mice.
(A) F4/80 immunohistochemical staining of liver sections from ApoE-/- mice. (B) The mRNA expressions of IL-1β, TNFα and MCP1 in livers of ApoE-/- mice (n = 6). (C) The protein expressions of IL-1β, TNFα and MCP1 in livers of ApoE-/- mice (n = 3). The histogram represents the densitometric scans for target protein bands normalized by β-actin and expressed as fold changes relative to protein expression in control mice. The results are depicted as mean ± SD, *P<0.05 versus control group, #P<0.05 versus casein injected alone group.
Fig 3.
Effect of atorvastatin on hepatic fibrosis in ApoE-/- mice.
(A) Sirius red staining of liver sections from ApoE-/- mice. (B) Quantitative analysis of Sirius red positive areas in separated fields from each group (n = 5). (C) The mRNA expression of αSMA, COL4 and TGFβ in livers of ApoE-/- mice (n = 6). (D) The protein expressions of αSMA, COL4 and TGFβ in livers of ApoE-/- mice (n = 3). The histogram represents the densitometric scans for target protein bands normalized by β-actin and expressed as fold changes relative to protein expression in control mice. The results are depicted as mean ± SD, *P<0.05 versus control group, #P<0.05 versus casein injected alone group.
Fig 4.
Effect of atorvastatin on the oxidative stress in livers of ApoE-/- mice.
(A) Superoxide anion (O2-) accumulation in liver cryosection analyzed by DHE staining (original magnification ×200). (B) Fluorescence intensity analysis of DHE staining. Values were expressed as the folds of control (n = 4). (C) Hepatic H2O2 levels (n = 4). (D) Hepatic MDA levels (n = 4). Data were expressed as mean ± SD. *P<0.05 versus control group, #P<0.05 versus casein injected alone group.
Fig 5.
Adaptive antioxidant response mediated by Nrf2 in livers of ApoE-/- mice after atorvastatin treatment.
(A) Immunohistochemical staining of Nrf2 in liver sections from ApoE-/- mice. (B) The protein expressions of Nrf2 in nucleus and cytoplasm fractions in livers of ApoE-/- mice (n = 3). (C) The mRNA expressions of HO-1, SOD2 and NQO1 in livers of ApoE-/- mice (n = 6). The enzymatic activity of (D) CAT and (E) SOD in livers of ApoE-/- mice (n = 4). The results are depicted as mean ± SD, *P<0.05 versus control group, #P<0.05 versus casein injected alone group.