experiment was similar to CYP2A6, which also indirectly proved that CYP2A6 expression was influenced by Nrf2. Is the gene of CYP2A5/2A6 located on a chromosome regulated by Nrf2? Whether Nrf2 is the sole compound regulates CYP2A6 in hepatocytes steatosis? Two putative stress response elements (StRE) within the promoter of mouse Cyp2a5 at positions −2514 to −2505 and −2386 to −2377 have been identified with computer-based sequence analysis, which may interact with Nrf2 (Abu-Bakar et al., 2007). In our study, the expression of Nrf2 and CYP2A6 showed inverse tendency in cells treated with increasing concentrations of LA, which indicated that Nrf2 was not the only pathway contributes to the increase of CYP2A6 induced by hepatic 18-carbon FA accumulation. An aryl hydrocarbon receptor (AHR)-dependent pathway has been reported to associate with the up-regulation of CYP2A5 and a putative AHR response element (XRE) was identified in the Cyp2a5 promoter at the position −2514 to −2492 using luciferase reporter gene assays (Arpiainen et al., 2005). In addition, the dexamethasone (DEX) induced CYP2A6 increase in human primary hepatocytes was attenuated by the glucocorticoid receptor (GR) antagonist, and a mutation of hepatic nuclear factor 4 (HNF4) alpha response element (HNF4-RE), which suggested that GR and HNF4
