In the present study, we found that STS can reduce CKD-enhanced leukocyte infiltration, blood and kidney ROS levels, renal 4-HNE expression, glomerulerosclerosis, tubulointerstitial fibrosis, Bax/caspase 3/PARP/apoptosis production, and GPX4/xCT mediated ferroptosis associated with the elevated urinary protein concentration, BUN and creatinine levels in the CKD kidneys, implicating STS reducing oxidative stress-induced inflammation, fibrosis, apoptosis and ferroptosis mechanisms in CKD. The gene discussed is BAX; the disease is chronic kidney disease.