Rapamycin Inhibit Acrole1n-induced Spermatogonial Stem Cells (SSCS) Damage Through Alleviating Oxidative Stress In Vitro

Acrolein level is possibly increased by several factors, such as lipid peroxidation, clinicalusage of cyclophosphamide (CP), fried food, automobile exhaust, smoking, and aging.Previous studies have indicated that acrolein caused intracellular oxidative stress (OS). TheOS, which plays an indispensable role in spermatogenesis and reproduction, is one of themain causes spermatogenesis disorders. Thus, we investigated the effects of acrolein in malegerm cell-derived GC-1cells, and further explored the reaction of OS and rapamycin in vitro.The results showed that acrolein caused OS. The OS decreased the ratio of Bcl2/Baxexpression level, which led to the vanishment of ΔΨm. The vanishment of ΔΨm led toapoptosis in SSCs. Rapamycin alleviated acrolein-induced OS and increased the ratio ofBcl2/Bax expression, which protected the mitochondrial membrane. In conclusion, rapamycininhibit acrolein-induced apoptosis through alleviating oxidative stress. More importantly, wefound inhibited mTORC1could relieve the cell aging caused by OS.