Research Article

Fenofibrate Ameliorates Hepatic Ischemia/Reperfusion Injury in Mice: Involvements of Apoptosis, Autophagy, and PPAR-α Activation

Figure 6

Possible mechanisms of fenofibrate during hepatic IR injury. In our IR-induced liver injury model, activated Kupffer cells promoted the release of proinflammatory cytokines such as TNF-α, IL-1β, and IL-6 and production of ROS. Fenofibrate can activate PPAR-α via phosphorylating AMPK, collaboratively regulating inflammation response, apoptosis, and autophagy downstream. Furthermore, AMPK activation increased accumulation of Nrf-2 to reduce ROS generation. FF shows hepatoprotective effects against IR injury by inhibiting inflammation and attenuating apoptosis and autophagy through the AMPK/PPAR-α pathway.