Taken together, these findings advance the understanding of mechanism associated with HBx and AFB1-induced hepatic necrosome formation, mitochondrial dysfunction and steatosis and make COX-2 a good candidate for treatment.
However, COX-2 activation in the epidydimal AT is strongly correlated with the development of AT inflammation, insulin resistance, and fatty liver in high-fat-diet-induced obese rats.
These results suggest that apoA-I overexpression can reduce steatosis by decreasing ROS levels and suppressing COX-2-induced inflammation in hepatocytes.