白消安致小鼠睾丸损伤的机理及其调控通路的研究进展

Research Progress on the Mechanism and Regulatory Pathway of Testicular Injury Induced by Busulfan in Mice

白消安因其具有较强精子毒害作用常被用于制备精原干细胞移植受体,但具体毒性机制尚不清楚,影响了其科学使用及效果提升。研究表明,白消安可引起生精细胞产生氧化应激、炎症反应,并抑制细胞自噬、损伤血睾屏障,毒害睾丸生精机能,但其相互之间的关系及调控通路尚不明确。基于核转录因子κB(nuclear transportation factorκB,NF-κB)通路在炎症反应中的重要调控作用,笔者综述了白消安引起的氧化应激、炎症反应,并损伤血睾屏障及抑制睾丸细胞自噬的研究结果,分析了NF-κB信号通路在白消安毒害睾丸中可能发挥的调控作用,以期深入揭示白消安毒害精子发生的分子机理,为科学使用白消安和避免环境毒素伤害提供参考。

Because of its strong toxic effect on spermatogonium,busulfan is often used to prepare spermatogonium stem cell transplantation recipients,but the specific toxic mechanism is still unclear,which affects its scientific use and effect improvement.Studies have shown that busulfan can cause oxidative stress and inflammatory response of spermatogenic cells,inhibit autophagy,damage blood-testis barrier,and poison spermatogenic function of testis,but the relationship between them and the regulatory pathway remain unclear.Based on the important regulatory role of nuclear transportation factorκB(NF-κB)pathway in inflammatory response,the author reviewed the research results of oxidative stress,inflammatory response,damage of blood-testis barrier and inhibition of testicular cell autophagy caused by busulfan,and analyzed the possible regulatory role of NF-κB signaling pathway in testicular toxicity of busulfan.The aim of this study was to reveal the toxic mechanism of busulfan to spermatogenesis,and to provide reference for scientific use of busulfan and to avoid environmental toxins.