In the present study, we further found that treatment with T-I at 30 mg/kg for 3 days significantly increased renal GSH levels and the activity of endogenous anti-oxidant enzymes, including SOD2 and CAT, in CDDP-treated mice, which demonstrated that T-I, as an anti-oxidant, could protect against CDDP-induced acute kidney injury in vivo. This evidence concerns the gene SOD2 and acute kidney injury.