中文摘要：

目的：探讨周围神经损伤时,微小RNA-21（microRNA-21,miR-21）与雪旺细胞（SC）凋亡的关系及相关分子机制。方法：采用实时荧光定量PCR（real-time PCR）检测动物模型中miR-21以及人第10号染色体缺失的磷酸酶及张力蛋白同源基因（phosphatase and tensin homologue deleted on chromosome 10,PTEN）的表达情况;通过将miR-21类似物（miR-21-mimic）、miR-21抑制物（miR-21-inhibitor）和阴性对照miRNA（negative control miRNA,NC-miRNA）转染入RSC96细胞中,构建出过表达miR-21的雪旺细胞株（MI-SC）、抑制miR-21表达的雪旺细胞株（IN-SC）及表达对照miRNA的雪旺细胞株（NC-SC）;采用流式细胞仪检测3组细胞的凋亡情况;real-time PCR检测3组细胞中miR-21以及PTEN的表达情况;Western blot检测3组细胞中PTEN及凋亡相关蛋白激活型caspase-3（cleaved caspase-3）的表达情况。结果：神经损伤组miR-21的表达量与对照组相比明显升高,神经损伤组PTEN mRNA的表达水平与对照组相比明显降低;与NC-SC相比,上调miR-21组细胞的凋亡比例减少,PTEN mRNA及蛋白的表达水平降低,cleaved caspase-3的表达水平降低,下调miR-21组细胞的凋亡比例增加,PTEN mRNA及蛋白的表达水平升高,cleaved caspase-3的表达水平升高（P〈0.05）。结论：miR-21可能通过下调PTEN的表达抑制雪旺细胞的凋亡,从而可能在周围神经的损伤修复中发挥作用。

英文摘要：

AIM： To explore the relationship and molecular mechanism between microRNA-21 （miR-21） and Schwann cells （SC） following peripheral nerve injury. METHODS： The mRNA expression of miR-21 and phosphatase and tensin homologue deleted on chromosome ten （PTEN） in animal model were detected by real-time PCR. The over-ex- pression of miR-21 and inhibition of miR-21 expression in the Schwann ceils according to transfection of lentiviral vectors were performed, the nonspecific miRNA was used as a negative control （NC）. The cell apoptosis was measured by flow cy- tometry. The mRNA expression of miR-21 and PTEN in the cells was detected by real-time PCR. The protein expression of PTEN and cleaved caspase-3 was determined by Western blot. RESULTS： The level of miR-21 was significantly higher and the mRNA level of PTEN was significantly lower in the model of nerve injury than those in control group, miR-21 over- expression decreased the number of apoptotic Schwann cells compared with NC-SC. The mRNA expression of PTEN was down-regulated by over-expression of miR-21. The protein expression of PTEN and cleaved caspase-3 was down-regulated by over-expression of miR-21 （P 〈 0.05 ）. CONCLUSION： miR-21 may play an important role in the peripheral nerve injury through inhibiting apoptosis of Sehwann ceils by down-regulating the expression of PTEN.