FIG 5.

AMPK is involved in the protective effects of CTRP9 on myocardial injury in vivo. (A) Phosphorylation of ACC and AMPK in the hearts of CTRP9-KO and WT mice 6 h after LPS or vehicle injection as assessed by Western blotting. (B) Phosphorylation levels of AMPK in the hearts of WT mice treated with Ad-CTRP9 or Ad-β-gal at 6 h after LPS injection. WT mice were systemically treated with Ad-CTRP9 or Ad-β-gal (3.0 × 10⁸ PFU total), followed by subjection to LPS injection. (C) Phosphorylation of ACC in the hearts of WT and dnAMPK-TG mice receiving Ad-CTRP9 or Ad-β-gal at 6 h after LPS injection. Ad-CTRP9 or Ad-β-gal (3.0 × 10⁸ PFU total) was delivered intravenously via the tail vein 5 days before LPS injection. Phosphorylation of ACC (pACC) was determined by Western blotting. (D) Quantitative analysis of the %FS in WT and dnAMPK-TG mice receiving Ad-CTRP9 or Ad-β-gal at 6 h after LPS injection. Ad-CTRP9 or Ad-β-gal (3.0 × 10⁸ PFU total) was delivered intravenously via the tail vein 5 days before LPS injection (n = 8 in each group). (E) Myocardial levels of TNF-α and IL-6 in WT (n = 6) and dnAMPK-TG (n = 5) mice at 6 h after LPS injection. mRNA levels of TNF-α and IL-6 were measured in the myocardium of WT and dnAMPK-TG mice that had received Ad-CTRP9 or Ad-β-gal by real-time PCR method and expressed relative to β-actin mRNA levels. The results are presented as means ± the SEM.