Fig. 3. AMPK alleviated UA-induced apoptosis and autophagy in UA-stimulated PTECs.

UA significantly increased reactive oxygen species (ROS) production (a, c) and early and late apoptosis (b, d, e); reduced cell viability (f); induced autophagy, as indicated by reduced p62 levels (g); and increased the LC3-II/LC3-I ratio (h) and beclin-1 levels (i). AICAR significantly attenuated ROS production (a, c), reduced early and late apoptosis (b, d, e), increased cell viability (f) and p62 levels (g), and showed a tendency to reduce beclin-1 levels (i) and the LC3-II/LC3-I ratio (h). Comp C increased ROS (a, c) and the LC3-II/LC3-I ratio (h). *P < 0.05 vs. Cont, **P < 0.01 vs. Cont, ^#P < 0.05 vs. UA, ^##P < 0.01 vs. UA