雌、孕激素对子宫内膜异位症裸鼠模型异位病灶中间隙连接蛋白26、32、43表达的影响

Effects of estrogen and progesterone on expressions of connexin26, connexin32 and connexin43 in nude mice model of endometriosis

目的:通过子宫内膜异位症在体模型,系统、完整地研究雌、孕激素对子宫内膜异位症异位内膜组织中间隙连接蛋白26(connexin 26,CX26)、CX32和CX43表达的影响。方法:建立子宫内膜异位症裸鼠模型,随机分为3组,即雌激素组(A组),孕激素组(B组)、对照组(C组)。于建模后7、14、21、28 d取裸鼠异位病灶,RT-PCR及Western blot分别检测3组异位病灶中CX26、CX32和CX43的表达。结果:异位病灶中CX26在A组表达增高,在B组表达降低,该A、B、C组相比其差异均有统计学意义(P=0.000);A组CX43较B、C组均降低,差异有统计学意义(P=0.000),B、C组之间CX43表达差异无统计学意义(P=0.621);A、B、C组异位病灶中均未能检测到CX32的表达。结论:①雌激素、孕激素对异位内膜组织中CX26的调节作用相反。②异位病灶中未能检测到CX32的表达,其对子宫内膜细胞间隙连接细胞间通讯(gap junction intercellular communication,GJIC)的影响及内膜的异位种植需待进一步研究。③雌激素可降低异位内膜组织中CX43的表达,孕激素对其无影响,推测雌激素可能通过降低CX43表达,降低内膜细胞GJIC功能,促进细胞异常增殖、分化,导致内膜异位种植能力提高。

Objective ：To observe effects of estrogen and progesterone on expressions of eonnexin26 （CX26）, eonnexin32 （CX32） and connexin43 （CX43） in nude mice model of endometriosis. Methods：Nude mice model of endometriosis was established. Totally 60 nude mice were randomly divided into three groups：estrogen group（group A）,progesterone group（group B） and control group （group C）. Mice of each group were killed on the 7th, 14th,21th,28th d randomly. Expressions of gene and protein（CX26,CX32,CX43） in endometriotic lesions were detected by RT-PCR and Western blot respectively. Results： Expressions of CX32 mRNA and protein were enhanced by estrogen （P=0.000）,but suppressed by progesterone. Expressions of CX43 mRNA and protein were strongly suppressed by estrogen（P=0.000）. But progesterone had no effect on expressions of CX43 mRNA and protein（P=0.621）. Expressions of CX32 mRNA and protein were not detected in any group. Conclusions：（1）Regulation of CX26 by estrogen and progesterone is opposite. （2） Expressions of CX32 mRNA and protein are not detected in any group,so their effects on gap junction intercellular communication （GJIC） and endometrial eetopic transplantation are not clear. （3）Expressions of CX43 mRNA and protein are strongly suppressed by estrogen. But progesterone had no effect on expressions of CX43 mRNA and protein. It is conjectured that estrogen could down regu- lation CX43, depress the function of GJIC, encourage abnormal cell proliferation and cell differentiation and enhance the ability of en- dometrial ectopic transplantation.