Representative blots show the JNK phosphorylation in liver (A), muscle (B) and adipose tissue (C) of sham and septic rats (upper panels).

<p>Total protein expression of JNK (A–C, lower panels). Phosphorylation of c-jun in liver (D), muscle (E) and adipose tissue (F) of sham and septic rats. Serine 307 Phosphorylation of IRS1 in liver (G), muscle (H) and adipose tissue (I) of sham and septic rats (upper panels). Total protein expression of IRS-1 (G–I, lower panels). Data are presented as means ± S.E.M from 6–8 rats per group. *P<0.05 (Sepsis/Sal vs. all others groups); **P<0.001 (Sepsis/Sal vs. control); #P<0.05 (Sepsis/Sal vs. Sepsis/Ator). IB, immunoblot; CLT: Sham/Saline; ShT: Sham/Atorvastatin; SAL: saline; ATOR: atorvastatin.</p

To evaluate the association of TLR4 with MyD88, immunoprecipitations were performed with MyD88 antibody followed by immunoblotting with TLR4 specific antibody.

<p>Representative blots show TLR4 activation (upper panels) and expression (lower panels) in liver (A), muscle (B) and adipose tissue (C) of sham and septic rats. IKKβ phosphorylation in liver (D), muscle (E) and adipose (F) of sham and septic rats. Total protein expression of IKKβ (D–F, lower panels). Phosphorylation of IκBα in liver (G), muscle (H) and adipose (I) of sham and septic rats. Data are presented as means ±S.E.M from 6–8 rats per group. *P<0.05 (Sepsis/Sal vs. all other groups); **P<0.001 (Sepsis/Sal vs. control); #P<0.05 (Sepsis/Sal vs. Sepsis/Ator). IB, immunoblot; CLT: Sham/Saline; ShT: Sham/Atorvastatin; SAL: saline; ATOR: atorvastatin.</p

Effects of atorvastatin treatment on insulin signaling in the CLP rat.

<p>Representative blots show insulin-induced tyrosine phosphorylation of Insulin Receptor β (IRβ) in liver (A), muscle (B) and adipose (C) of sham and septic rats. Total protein expression of IRβ (A–C, lower panels). Insulin-induced tyrosine phosphorylation of Insulin Receptor Substrate 1 (IRS1) in liver (D), muscle (E) and adipose tissue (F) of sham and septic rats. Total protein expression of IRS1 (D–F, lower panels). Insulin-induced serine phosphorylation of Akt in liver (G), muscle (H) and adipose (I) of sham and septic rats. Insulin-induced threonine phosphorylation and total protein expression of Akt (G–I, lower panels). In this case, blots were stripped and reprobed with β-actin (A–I, lower panels) to confirm equal loading of proteins. Data are presented as means +/− S.E.M from 6–8 rats per group. *P<0.05 (Sepsis/Sal vs. all others groups). IB, immunoblot; CLT: Sham/Saline; ShT: Sham/Atorvastatin; SAL: saline; ATOR: atorvastatin.</p

Representative blots show the NFkB activation in nuclear fractions of liver (A), muscle (B) and adipose tissue (C) of sham and septic rats.

<p>In this case blots were stripped and reprobed with actin (A–C, lower panels) to confirm equal loading of proteins. Tissue levels of iNOS (D–F) and IL-6 (G–I) expression in liver, muscle and adipose tissue of sham and septic rats. Data are presented as means ± S.E.M from 6–8 rats per group. *P<0.05 (Sepsis/Sal vs. all others groups); **P<0.001 (Sepsis/Sal vs. control); #P<0.05 (Sepsis/Sal vs. Sepsis/Ator). IB, immunoblot; CLT: Sham/Saline; ShT: Sham/Atorvastatin; SAL: saline; ATOR: atorvastatin.</p

Effect of atorvastatin on survival in CLP sepsis model.

<p>Male Wistars rats, 8 weeks old, were given saline (Sepsis/Sal, n = 20) or atorvastatin 10 mg/kg (Sepsis/Ator, n = 20), 3 h and once a day after CLP. Survival of the rats was monitored at intervals of 12 h for 15 days. The overall difference in survival rate between the groups with and without atorvastatin was significant (P<0.0001) (A). Fasting blood glucose (B). Fasting insulin levels (C). Glucose disappearance rate (D). HOMA-IR index (E). Serum levels of TNF-α (F) and IL-6 (G). Data are presented as means and S.E. of six to eight rats per group. *P<0.05 (Sepsis saline vs. all others groups).</p