Figure 11. Schematic diagram of proposed mechanism by which Carminic acid alleviates fructose-induced kidney injury. On the basis of our findings in this study and our published data in the study of chronic kidney injury, we proposed that Fru could induce glucose disorder, dyslipidemia, AMPKα inactivation and fibrosis in renal tissues of mice. In addition, we showed that Fru treatment led to significant inflammatory response in cells and in kidney tissues of mice through promoting the activation of NF-κB and JNK signaling pathways. Moreover, oxidative stress was also induced by Fru both in vitro and in vivo. Notably, we found that CA treatment could reverse all these events caused by Fru, alleviating chronic kidney injury consequently. Importantly, we demonstrated that CA-alleviated inflammation and oxidative stress were mainly dependent on Nrf2 activation.