The main findings were the following ones: (i) the BBR treatment could impair liver steatosis, lobular inflammation, hepatocyte ballooning, and NAS score; (ii) BBR could enhance the expression of Clock and Bmal1; (iii) BBR mitigated the redox imbalance mediated liver inflammation by decreasing the production of ROS and H2O2; (iv) the glucose metabolism regulated by BBR was depending on the cyclic expression of Bmal1 gene. Here, BMAL1 is linked to fatty liver disease.