AKT1 and glomerulosclerosis: Hsu considered that BBR inhibited the action of OS by inhibiting Nrf-2 pathway and the activities of AMP-activated protein kinase (AMPK), PI3K/Akt, and p38 pathway, and activated the expression of antioxidant enzymes such as superoxide dismutase and glutathione, which delayed the formation of glomerulosclerosis and finally the process of renal fibrosis (38).