目的 探讨骨髓间充质干细胞(MSCs)来源的白介素-6 （IL-6）对神经细胞损伤的作用。方法 构建大鼠沉默IL-6 （siIL-6）慢病毒，感染MSCs，嘌呤霉素筛选siIL-6-MSCs稳定细胞株。Real-Time PCR和Western blotting检测细胞IL-6 mRNA和蛋白表达变化，ELISA检测siIL-6-MSCs培养上清液中IL-6分泌水平。将siIL-6-MSCs细胞与氧糖剥夺（OGD）损伤的PC12细胞分离共培养，Annexin V-FITC/PI法检测损伤细胞凋亡，Western blotting检测细胞中IL-6信号通路关键蛋白STAT3以及凋亡相关因子Bax和Bcl-2蛋白的表达。结果 siIL-6干扰序列正确插入慢病毒质粒中。siIL-6慢病毒感染MSCs后，IL-6 mRNA和蛋白表达及IL-6分泌水平均显著降低。与siIL-6-MSCs分离共培养后，OGD损伤的PC12细胞凋亡增加，STAT3、Bcl-2蛋白表达显著降低，Bax蛋白表达显著升高。结论 MSCs来源的IL-6可能通过STAT3信号通路，调节OGD损伤PC12细胞的抗凋亡作用。

Objective To investigate the effects of mesenchymal stem cells (MSCs) originated interleukin-6 (IL-6) on the nerve cells injury. Methods The rat siIL-6 recombinant lentivirus plasmid was constructed and the siIL-6 recombinant lentivirus was infected by MSCs. The MSCs cell line with stable siIL-6 expression was selected by puromycine. The variations of IL-6 mRNA and protein expression levels were detected by the Real-Time PCR and Western blotting. The secretion level of IL-6 was detected from the cultured supernatant of siIL-6-MSCs by the ELISA. The siIL-6-MSCs cells and PC12 cells injured by oxygen glucose deprivation (OGD) were separated and co-cultured. Cell apoptosis was detected by the Annexin V-FITC/PI. Expressions of key protein STAT3 of IL-6 signaling pathway and apoptosis related factors Bax and Bcl-2 were detected by the Western blotting. Results The IL-6 siRNA sequence was correctly cloned to the lentivirus plasmid. Expression levels of IL-6 mRNA and protein and the secretion level of IL-6 significantly decreased after MSCs were infected by the siIL-6 lentivirus. After being separated and co-cultured with siIL-6-MSCs, the apoptosis of OGD injured PC12 cells increased; protein expression levels of STAT3 and Bcl-2 significantly decreased; and the protein expression of Bax significantly increased. Conclusion MSCs-originated IL-6 may regulate the anti-apoptotic function of OGD injured PC12 cells through the STAT3 signaling pathway.