Figure 8
UA-8-triggered phosphorylation of AMPK and modulation of the autophagic response in starved HL-1 cells and NCMs were abolished by cotreatment with HMR-1098. The increased phosphorylated AMPK (Thr172) correlated with UA-8-activated autophagic response following 24 h of starvation in HL-1 cells (a) and NCMs (b), which was detected by western blot. The relative changes in phosphorylated AMPK and LC3-II expression levels were quantified in HL-1 cells and NCMs following treatments after 24 h of starvation and are presented below as respective representative western blots. Values are represented as mean±S.E.M., N=3. Significance was P<0.05, *significantly different from control nonstarvation, #significantly different from UA-8. (c) A general scheme illustrating a hypothesis for EET-mediated protective effects. Increased levels of EETs can shift cell death pathways from apoptotic and necrotic responses, which result in cell loss, to an autophagic pathway, resulting in cell survival. Autophagy may enhance turnover of damaged molecules and organelles, such as mitochondria, increasing survivability
