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作 者:韩妍[1] 李莉[1] 王赞宏[1] 李风艳[1] 侯红丽[1] 张亚琴[1]
机构地区:[1]山西医科大学第一附属医院妇科,太原030001
出 处:《中国药物与临床》2008年第4期286-289,共4页Chinese Remedies & Clinics
基 金:山西省科技厅攻关基金资助项目(042024-2)
摘 要:目的探讨米非司酮对体外培养子宫腺肌病在位内膜中腺上皮细胞的增殖及凋亡的影响。方法用反转录聚合酶链反应半定量分析Ki-67 mRNA和Caspase-3 mRNA在病例组、药物干预组、对照组(肌瘤组)子宫内膜腺上皮细胞的表达。结果病例组增生期和分泌期腺上皮细胞均较对照组表达Ki-67 mRNA增强(P<0.05)。用米非司酮药物干预后Ki-67 mRNA表达下降。病例组增生期腺上皮细胞Caspase-3 mRNA表达较对照组明显下降(P<0.05),而病例组分泌期腺上皮细胞Caspase-3 mRNA表达与对照组差异无统计学意义(P>0.05)。用米非司酮药物干预后,病例组增生期腺上皮细胞Caspase-3 mRNA表达增强(P<0.05),而分泌期腺上皮细胞Caspase-3 mRNA表达没有明显增强(P>0.05)。结论子宫内膜腺上皮细胞凋亡与增殖失衡可能是子宫腺肌病的发病机制之一,米非司酮可诱导子宫内膜腺上皮细胞凋亡,抑制内膜腺上皮细胞增殖,从而控制子宫腺肌病的发展。Objective To explore effects of mifepristone intervention on proliferation and apoptosis of cultured glandular cells from entopic endometrium in adenomyosis. Methods The expressions of Caspase-3 mRNA and Ki-67 mRNA in these cells were detected with semi-quantitative RT-PCR. Results Compared with control group, higher level of Ki-67 mRNA expression in the glandular cells was found in adenomyosis group than in control group during both proliferative and secretory phases (P〈0.05). The expression of Ki-67 mRNA was decreased 'after intervention with mifepristone (P〈0.05). During proliferative phase, the expression of Caspase-3 mRNA in the glandular epithelium cells of adenomyosis group was weaker than that in control group (P〈0.05), but no difference was observed during the secretory phase (P〉0.05). In proliferation phase, the expression of Caspase-3 mRNA in mifepristone group was stronger than that in adenomyosis group (P〈0.05), but again, the two groups did not differ during the secretory phase. Conclusion Disturbance of apoptosis and proliferation in glandular epithelium cell from endometrium in adenomyosis may be involved in the pathogenesis of adenomyosis. Mifepristone was shown to induce apoptosis and inhibit proliferation of glandular epithelium cells from endometrium, hence providing control of adenomyosis.
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