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

Figure 9 Western blot analysis was performed for Beclin-1, LC3-II, p-AMPK, p-ULK1, and p-mTOR in IEC-6 cells in the Sham, lipopolysaccharide, lipopolysaccharide + esmolol, lipopolysaccharide + 3-methyladenine, and lipopolysaccharide + rapamycin treatment groups (after 6 hours of treatment). A-D: Protein levels of Beclin-1, LC3-II, p-mTOR and β-Actin were determined by western blotting. The representative blots of Beclin-1, LC3-II, p-AMPK, p-ULK1, and p-mTOR and β-actin after treatment. β-actin was used as loading control and for normalization; E-G: Protein levels of p-AMPK, p-ULK1 and βActin were determined by western blotting. 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.