干细胞微囊对大鼠Leydig细胞急性氧化应激损伤的保护机制研究

Mechanisms of stem cell-derived extracellular vesicles protecting Leydig cells from acute oxidative injury in rats

目的:揭示干细胞微囊改善Leydig细胞急性氧化应激损伤的机制。方法:实验组采用单侧睾丸切除的SD大鼠5例建立睾丸缺血-再灌注损伤模型,经尾静脉注射干细胞微囊进行干预。对照组采用单侧睾丸切除的SD大鼠5例经尾静脉注射等量PBS。再灌注2 h后HE染色检测睾丸组织中中性粒细胞浸润程度,TUNEL和caspase 3免疫组化染色检测Leydig细胞凋亡,Ki67免疫组化染色检测Leydig细胞增殖。结果:实验组大鼠睾丸间质血管中中性粒细胞黏附明显少于对照组,且TUNEL及caspase 3免疫组化结果显示Leydig细胞的凋亡数量明显少于对照组,Ki67免疫组化结果显示实验组Leydig细胞增殖数量多于对照组。结论:干细胞微囊可减少中性粒细胞在急性期的黏附,通过减少活性氧自由基的来源改善Leydig细胞的急性氧化应激损伤。

Objective ： To investigate the mechanisms of stem cell-derived extracellular vesicles （EVs） alleviating acute oxi- dative stress injury to Leydig cells. Methods ： The model of testicular ischemia-reperfusion was established by unilateral testicu- lar resection in l0 SD rats followed by injection of EVs into the tail vein in 5 of the animals （the experimental group） and that of iso- tonic PBS in the other 5 （the control group）. At 2 hours after reperfusion, the infiltration of neutrophilsin the testicular tissue was de- tected by HE staining, the apoptosis of Leydig cells measured by TUNEL and Caspase-3 immunohistochemistry, and the proliferation of Leydig cellsdetermined by Ki-67 immunohistochemical staining. Results ： Compared with the control, the experimental group showed significantlymilderinfihration of neutrophils in the interstitial tissueof the testis and lower apoptosis and higher proliferation of Leydig cells. Conclusion ： Stem cell EVs can reduce the adhesion of neutrophils in the acute phase and alleviate acute oxida- tive stress injury to Leydig cells by decreasing the production of reactive oxygen free radicals.