FIG 6.

The model of Nrf2-mediated repression of antioxidant responses in RHDV-infected livers. First, Keap1 interacts with NF-κB (p50/p65) to form a complex in liver cells. RHDV infection induces oxidative stress in livers, and the Keap1-p50/p65 complex translocates into the nucleus to facilitate the dissociation of Nrf2 from the ARE. Then, the Keap1-Nrf2 complex separates from p50/p65 and is exported from the nucleus. Finally, ubiquitination and degradation of Nrf2, mediated by Keap1, occur. In addition, activation of Nrf2 by the antioxidant tBHQ upregulates defensive genes that protect cells from oxidative stress.