The changes of CYP2A5 protein expression and Nrf2 nuclear translocation showed the same trend in HFD fed WT mice liver compared to the control mice (Figure 2). Considering the hepatic FA accumulation (Wang X. et al., 2016), the increase of CYP2A5 protein expression and Nrf2 nuclear translocation in HFD-WT mice demonstrated that HFD-induced FA accumulation up-regulated CYP2A5 and activated Nrf2. However, the hepatic CYP2A5 protein expression in HFD-Nrf2-null mice approached to the basal level in mice fed with CD. This phenomenon indicated that expression of Nrf2 is crucial for the up-regulation of mouse hepatic CYP2A5 induced by HFD feeding. Another research based on mice exposed to cadmium chloride (16 mmol/kg body weight) reported that cadmium alters cellular redox status, induced hepatic CYP2A5 in WT mice but not in Nrf2-null mice (Abu-Bakar et al., 2004). Our study is in agreement with the above finding that Nrf2 may be the common regulator which contributes to the up-regulation of CYP2A5 in liver injuries induced by structurally irrelevant pathogenesis. Our data also showed that in Nrf2-null mice, the increase of CYP2A5 induced by hepatic
