Insl3基因缺失与睾丸扭转的关系

Relationship between loss of Insl3 and testicular torsion

目的探讨Insl3基因缺失与睾丸扭转的关系。方法分别取青春前期(出生后23 d,P23)及成年小鼠(出生后90d,P90)的野生型(WT)、杂合子(Het)及Insl3基因敲除(KO)小鼠,使用显微镜观察睾丸的位置、形态及精索的形态、长度。结果 Insl3 KO小鼠睾丸扭转发生率(3.94%),明显高于Het组(1.25%)及WT组(0)(P<0.05);精索形态异常在KO组与WT组有显著差异(64.38%vs 0,P<0.001);在各年龄组,Insl3 KO小鼠比WT及Het小鼠精索长度明显增长(P<0.05),但WT和Het小鼠之间无显著差异(P>0.05)。结论 Insl3基因敲除小鼠的精索、睾丸解剖异常明显增加,睾丸扭转率增高。Insl3激素缺失与睾丸扭转的发生关系密切。

Objective To explore the relations between loss of Insl3 gene and testicular torsion.Methods The appearance and location of testis,and the length and morphology of spermatic cord were observed in wild type（WT）,Insl3 heterozygous（Het） and Insl3 knockout mice（KO） at postnatal day 23（P23） and at adulthood（postnatal day 90,P90） under a microscope.Results The incidence rate of testicular torsion in KO mice（3.94%） was significantly higher than that in Het mice（1.25%） and WT mice（0）（P0.05）.Morphologically abnormal rate of spermatic cord was significant higher in KO mice than that in WT mice（64.38% vs 0,P0.001）.The length of spermatic cord was longer in KO mice than those in WT mice and Het mice of both two ages（P0.05）,but there was no difference in length of spermatic cord between WT mice and Het mice（P0.05）.Conclusion Insl3 KO mouse manifesties more anatomical abnormalities on spermatic cord and testis and higher rate of testicular torsion.The results suggest that the loss of Insl3 may cause testicular torsion.