〔Abstract〕 Objective To investigate the effect of CD147 on reducing hydrogen peroxide-induced oxidative stress injury in prostate cancer LNCaP cells. Methods The lentiviral system was used to establish a CD147-silencing prostate cancer cell model(LNCaP/shCD147 cells) and a negative control cell(LNCaP/Scramble cell), and RT-qPCR was performed for verification.By detecting the activity of reactive oxygen species(ROS), superoxide dismutase(SOD), glutathione peroxidase(GSH-PX) and malondialdehyde(MDA) in LNCaP/shCD147 and LNCaP/Scramble cells to verify the changes of oxidative stress and antioxidant enzymes in prostate cancer cells after silencing CD147; hydrogen peroxide(H2O2) was added to the cells and the cell growth was detected by CCK-8; Western blot was used to detect the expression changes of nuclear factor E2 related factors(Nrf2) and heme oxygenase-1(HO-1) to verify the relationship between the oxidative stress that occurs in prostate cancer cells after silencing CD147 and the PI3 K/AKT signaling pathway. Results Successfully constructed a CD147-silencing prostate cancer cell model. Compared with LNCaP/Scramble cells, the expression of CD147 in mRNA was reduced(P<0.01).The results of oxidative stress showed that the content of ROS and MDA in cells increased after silencing CD147(ROS,P<0.01; MDA,P<0.05), while the activities of SOD and GSH-PX decreased(P<0.01), indicating that after silencing CD147, LNCaP/shCD147 cells undergo oxidative stress. In addition, with the increase of H2O2concentration, the survival rate of LNCaP/shCD147 group cells decreased(P<0.01). After inhibiting the PI3 K/AKT signaling pathway, the expressions of Nrf2 and HO-1 in the LNCaP/shCD147 group were reduced(P<0.01), indicating that CD147 inhibits the oxidative stress injury of prostate cancer cells through the PI3 K/AKT pathway. Conclusion CD147 can reduce the oxidative stress damage of PCa cells, and its inhibitory mechanism may be related to the PI3 K/AKT signaling pathway.