Furthermore, it was demonstrated that SAL could suppress oxidative stress-induced pulmonary fibrosis, cardiomyocyte injury and necrosis, and cerebral ischemia/reperfusion injury, by promoting transcription of Nrf2-regulated genes (HO-1 and NQO1), thus decreasing excessive production of ROS and improving mitochondrial function [42,43,44,45,46]. This evidence concerns the gene NQO1 and pulmonary fibrosis.