Reactive oxygen species (ROS) are important in the development of diabetic testicular dysfunction. Overproduction of ROS promotes the process of apoptosis, which shows that there is a crosstalk between oxidative stress and apoptosis. Recent research has suggested that NADPH oxidase is the main source of ROS. In this study, we investigated whether the NADPH oxidase inhibitor, apocynin, can improve diabetesâinduced testicular dysfunction by suppressing oxidative stress. The streptozocin (STZ)-induced diabetic rats were administered apocynin, and the mRNA and protein expression of Bax, Bcl-2, p47phox and p67phox was examined by real-time PCR (RT-PCR) and western blot analysis. Production of ROS was measured by thiobarbituric acid reactive substances (TBARS) assay. Terminal-deoxynucleoitidyl transferase mediated nick end-labeling (TUNEL) assay was used to detect apoptosis and ELISA was used to detect total testosterone levels. The mRNA and protein expression of Bcl-2 was signiïŹcantly reduced, and that of Bax, p47phox and p67phox was signiïŹcantly increased in the diabetic rats compared to the control group. Apocynin signiïŹcantly increased the expression of Bcl-2 and decreased the expression of Bax, p47phox and p67phox at both the mRNA and protein levels. The production of ROS and apoptotic cells signiïŹcantly increased in the diabetic group compared to the control group. Apocynin signiïŹcantly reduced the production of ROS and apoptotic cells and increased the total testosterone level. In conclusion, apocynin is capable of ameliorating testicular dysfunction.