Objective: To investigate the relationship between the nuclear translocation of peroxiredoxin 4 (PRDX4) in ovarian granulosa cells (GCs) and the cell senescence phenotype in aging state. Methods: The ovarian tissues of 6-week-old(young group) and 9-month-old (aged group) female C57BL/6 mice were taken for immunofluorescence staining to observe the nuclear translocation of PRDX4 in GCs. At the same time, human ovarian granulosa cell line KGN was cultured, and thapsigargin(Tg) was used to induce the establishment of in vitro aging model. The optimal induction conditions were screened by CCK-8 assay. The expression levels of senescence-related proteins (P16, P21, P53) and senescence-associated secretory phenotype (SASP)factors[interleukin(IL)-1α, IL-1β, IL-6, IL-8] were detected by western blot and (real-time quantitative PCR, RT-qPCR) to validate the aging model. On this basis, the effect of the senescence phenotype on the nuclear translocation of PRDX4 was further examined. Results: Immunofluorescence results showed that compared with the young group, the fluorescence signal in the nucleus of PRDX4 in the ovarian GCs of the aged group was significantly enhanced(P < 0.01). In vitro, PRDX4 was mainly localized in the cytoplasm of normal KGN cells. After Tg-induced aging, the expression levels of P16, P21, and P53 proteins in the aging group were significantly increased(all P < 0.05), and the mRNA expression levels of SASP-related factors were also significantly up-regulated(P < 0.001), confirming that the aging model was successfully constructed. Nuclear-cytoplasmic separation experiments further showed that the content of PRDX4 protein in the nucleus of the aging group was significantly higher than that in the young group(P < 0.01), while the corresponding decrease in the cytoplasm indicated that PRDX4 was translocated from the cytoplasm to the nucleus. Conclusion: Aging can induce the translocation of PRDX4 from cytoplasm to nucleus in ovarian GCs and its nuclear translocation may be involved in the regulation of ovarian aging.