Catalpol-Induced AMPK Activation Alleviates Cisplatin-Induced Nephrotoxicity through the Mitochondrial-Dependent Pathway without Compromising Its Anticancer Properties

Figure 8

Schematic illustration of the signaling pathway involved in the effect of CAT on cisplatin-induced nephrotoxicity in vitro. CAT activated AMPK activity and improved mitochondrial function, decreased cellular ROS generation, and increased ATP production, leading to reduced inflammation and apoptosis as well as activation of mitophagy, which ultimately protected against cisplatin-induced injury.