目前全球不孕不育发生率约为15%，男性因素约占50%，氧化应激是重要诱因之一。但精原干细胞氧化还原平衡的调控机制尚不清楚。前期预实验提示过氧化物氧化还原蛋白（Peroxiredoxin-1，PRDX1）在非梗阻性无精症患者睾丸中的表达显著下降。同时提示PRDX1主要表达于精原干细胞，以巯基依赖的方式与干细胞因子c-Myc结合；敲低Prdx1后，c-Myc表达下降，精原干细胞呈现分化加速迹象。精原干细胞缺失Prdx1的小鼠生精小管严重萎缩，出现无精症。我们设想：PRDX1可能以巯基氧化还原的方式调控c-Myc维持精原细胞种群平衡以及精子发生顺利进行。本课题拟利用精原干细胞Prdx1敲除和过表达小鼠，及精原干细胞体外培养体系，结合TBHP诱导氧化应激模型，从分子、细胞和整体水平探讨PRDX1在精原干细胞氧化还原平衡、自我更新和分化及精子发生中的作用和机制，为男性不育的防治提供实验依据。

Epidemiological data indicate a 15% infertile incidence around the world, of which the male factor accounts for about 50%, and oxidative stress is one of the critical cause. However, the regulatory mechanism of redox balance in spermatogonial stem cells is still unclear. Our preliminary experimental results indicated that the expression of peroxiredoxin-1 (PRDX1) in testis of patients with non-obstructive azoospermia was significantly decreased. The results also showed that PRDX1 was predominantly expressed in spermatogonial stem cells and binded to stem cell factor c-Myc in a thiol-dependent manner. When Prdx1 was knocked down, decreased expression of c-Myc and accelerated differentiation of spermatogonial stem cells were observed. Besides, the mice with Prdx1 deficiency in spermatogonial stem cell demonstrated severely atrophied seminiferous tubules and azoospermia. Thus, we hypothesized that PRDX1 maintains the balance of spermatogonial self-renewal and differentiation and spermatogenesis by thiol-redox regulation of c-Myc. In this study, we intend to explore the role and mechanism of PRDX1 in redox balance, self-renewal and differentiation of spermatogonial stem cells and spermatogenesis at the molecular, cellular and whole levels, by using spermatogonial stem cell-specific Prdx1 deletion and overexpression mice and in vitro cultured spermatogonial stem cell, combined with TBHP-induced oxidative stress model, aiming to provide experimental basis for the prevention and treatment of male infertility.