Oxidative stress is one of the main causes of testicular spermatogenesis disorders. Resveratrol (RES) can inhibit oxidative stress levels, reduce germ cell damage, and promote spermatogenesis. To investigate the molecular mechanism by which RES promotes spermatogenesis, the effects of hydrogen peroxide (H2O2) on the pathological damage of mouse testis tissue were assessed. The expression of key genes associated with pyroptosis, apoptosis, and autophagy, and the effects of RES on this process were determined. Experimental mice were divided into three groups with intraperitoneally injection of H2O2 (3 mmol/kg/d), RES (100 mg/kg/d) + H2O2 (3 mmol/kg/d), and normal saline, respectively. The testicular tissues were collected, and the pathological changes were observed by hematoxylin and eosin staining. The ultrastructure was observed using transmission electron microscopy (TEM). The transcriptional levels of pyroptosis, apoptosis, and autophagy-related genes were measured and analyzed by fluorescence quantitative polymerase chain reaction. The results showed that, in the H2O2 group, the basal membrane of spermatogenic tubules was damaged, atrophic, and thin. Interstitial cells were fragmented, and the gap of spermatogenic tubules increased. Compared with the H2O2 group, the pathological damage of testicular tissue structure in the H2O2 + RES group was significantly ameliorated. TEM results showed no evident damage to the cell structure in the control group, while apoptosis, autophagy, and pyroptosis were observed in the testicular tissue of H2O2 and H2O2 + RES groups, where cell damage was less, but apoptotic bodies, autophagosomes, and pyroptosomes were observed. The transcription levels of key pyroptosis genes increased in the H2O2 group but decreased significantly after RES treatment. The results indicated that H2O2 could induce pyroptosis, while RES inhibited pyroptosis and led to the release of inflammatory factors by regulating the expression of genes in signaling pathways. After H2O2 injection, the transcript levels of key apoptosis genes in testicular tissue were lower than those in the control group, while RES promoted the occurrence of H2O2-induced apoptosis, to achieve the purpose of protecting itself from oxidative damage. H2O2 could promote autophagy in mouse testicular tissue. RES enhanced the level of H2O2-induced autophagy, removed the damaged cells in the testicular tissue, and protected the development of the body. This study provided the experimental basis for the study of RES in oxidative damage, pyroptosis, apoptosis, and autophagy, and theoretical guidance and new ideas for drug development and treatment of male reproductive diseases in clinical practice. [ABSTRACT FROM AUTHOR]