Furthermore, vitamin C almost completely blocked the G2/M arrest induced by DBP, and the expression of α-SMA, fibronectin and TGF-β in NRK49F cells decreased to some degree when the cells were pretreated with vitamin C. In addition, TGF-β overproduction in NRK52E cells induced by DBP could be reversed by vitamin C. Together, these findings suggest that the oxidative stress induced by DBP can activate renal fibroblasts, increase the G2/M phase arrest of tubular epithelial cells, and promote progression of renal fibrosis. Here, ACTA1 is linked to renal fibrosis.