MiR-32-5p aggravates intestinal epithelial cell injury in pediatric enteritis induced by Helicobacter pylori

Figure 3 Transforming growth factor-β1/p38 participates in apoptosis of intestinal epithelial cells infected by Helicobacter pylori. A: Apoptosis detection in transforming growth factor-β1 (TGF-β1)-treated intestinal epithelial cells in the presence of transforming growth factor-β-activated kinase 1 (TAK1) inhibitor and p38 inhibitor; B: Protein levels of total TAK1, p38, phosphorylated TAK1, and phosphorylated p38 in TGF-β1-treated intestinal epithelial cells in the presence of TAK1 inhibitor and p38 inhibitor; C: Cell viability measurement in Helicobacter pylori (H. pylori)-infected intestinal epithelial cells with TAK1 inhibitor and p38 inhibitor treatment followed by transfection with miR-32-5p mimic; D: Cell viability measurement in H. pylori-infected intestinal epithelial cells with TAK1 inhibitor and p38 inhibitor treatment followed by transfection with miR-32-5p inhibitor; E: Apoptosis evaluation in H. pylori-infected intestinal epithelial cells with TAK1 inhibitor and p38 inhibitor treatment followed by transfection with miR-32-5p mimic; F: Apoptosis evaluation in H. pylori-infected intestinal epithelial cells with TAK1 inhibitor and p38 inhibitor treatment followed by transfection with miR-32-5p inhibitor. ^bP < 0.01, ^dP < 0.01, ^fP < 0.01, ^gP < 0.05, ^hP < 0.01. TGF-β1: Transforming growth factor-β1; TAK1: Transforming growth factor-β-activated kinase 1; H. pylori: Helicobacter pylori.