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目的:利用慢病毒介导特异性短发夹状RNA(LV-shRNA)靶向沉默生存素基因,观察其对子宫内膜异位症裸鼠模型异位病灶中caspase-3表达的影响。方法:建立人子宫内膜裸鼠皮下种植模型,将LVshRNA、空载慢病毒及磷酸盐缓冲液分别注射至裸鼠皮下异位病灶,观察病灶生长情况。分别采用RT-PCR及免疫组化检测异位病灶中生存素、caspase-3 mRNA及蛋白的表达。结果:LV-shRNA处理组病灶体积、重量明显低于两对照组。与两对照组相比,LV-shRNA处理组生存素mRNA及蛋白的表达量明显降低,caspase-3的表达量明显升高,而生存素及caspase-3的表达在两对照组之间相比,差异均无统计学意义。结论:LVshRNA可明显抑制裸鼠异位子宫内膜病灶的生长,其机制可能与其通过下调生存素蛋白、激活下游的caspase-3诱导细胞凋亡有关。
OBJECTIVE: To use lentivirus-mediated short hairpin RNA (shRNA-shRNA) to target survivin gene silencing and investigate its effect on the expression of caspase-3 in ectopic lesions of endometriosis nude mice. Methods: Human uterine epithelial cells were subcutaneously implanted in nude mice. LVshRNA, empty lentivirus and phosphate buffer were injected into the subcutaneous ectopic lesions of nude mice respectively to observe the growth of the lesions. RT-PCR and immunohistochemistry were used to detect the expressions of caspase-3 mRNA and protein in ectopic lesions. Results: The volume and weight of lesion in LV-shRNA treated group were significantly lower than those in the two control groups. Compared with the two control groups, the expression of survivin mRNA and protein in LV-shRNA treatment group was significantly decreased, and the expression of caspase-3 was significantly increased, while the expression of survivin and caspase-3 in the two control groups , The difference was not statistically significant. CONCLUSION: LVshRNA can significantly inhibit the growth of ectopic endometrial lesion in nude mice, which may be related to its mechanism by down-regulating survivin and activating downstream caspase-3.