Esmolol alleviates lipopolysaccharide-induced intestinal injuries by enhancing autophagy through the AMPK/mTOR/ULK1 pathway

Figure 6 Western blotting was performed for Beclin-1, LC3-II, p-AMPK, p-ULK1, and p-mTOR in intestinal tissue homogenates in the Sham, lipopolysaccharide, lipopolysaccharide + esmolol, lipopolysaccharide + 3-methyladenine, and lipopolysaccharide + rapamycin treatment groups (after 12 and 24 hours of treatment). A-C: The 12-hour protein levels of Beclin-1, LC3-II and β-Actin were determined by western blotting of each group; D-F: The 24-hour protein levels of Beclin-1, LC3-II and β-Actin were determined by western blotting of each group; G-J: The 12-hour protein levels of p-AMPK, p-ULK1, p-mTOR and β-Actin were determined by western blotting of each group; K-N: The 24-hour protein levels of p-AMPK, p-ULK1,p-mTOR and β-Actin were determined by western blotting of each group.β-actin was used as a loading control and for normalization. Representative immunoblots and densitometry analyses are presented. Data in the Sham group were set to 1. n = 6 in each group. 3-MA: 3-methyladenine; ES: Esmolol; RAPA: Rapamycin; LPS: Lipopolysaccharide.