多囊卵巢综合征患者卵泡基底膜超微结构的研究

Ultrastructure of basal lamina of follicles in polycystic ovary syndrome

运用透射电镜观察多囊卵巢综合征(PCOS)组及正常妇女组卵泡的形态,用体视学方法测量两组各级卵泡基底膜的厚度。结果显示:两组原始卵泡的基底膜厚度相似,但随着卵泡的发育卵泡基底膜逐渐增厚,PCOS组增厚更明显,对照组初级卵泡基底膜的平均厚度是0 293±0 204μm,PCOS组是0 463±0 287μm,两组比较有统计学差异(P<0 05)。对照组次级卵泡基底膜的平均厚度为0 542±0 298μm,PCOS组为1 234±0 345μm,两组比较有统计学差异(P<0 05)。两组原始卵泡的前颗粒细胞的超微结构相似,随着卵泡的发育,PCOS组的颗粒细胞内参与蛋白质合成的细胞器明显较对照组丰富;正常组窦前卵泡的颗粒细胞出现分化现象,PCOS组却未见分化现象。结果提示:PCOS患者卵泡基底膜屏障的增厚可能使卵泡刺激素FSH进入卵泡困难,颗粒细胞不能正常分化,"FSH 颗粒细胞轴"功能低下,导致不孕症。

Transmission electron microscopy was used to study the follicular morphology of polycystic ovary syndrome (PCOS) and normal women. Sterology method was used to measure the thickness of basal lamina of granulosa cells of follicles in each stage. It was found that the thickness of basal lamina of granulosa cells of primordial follicles had no difference between two groups(P>0.05). The thickness of basal lamina of granulose cells of follicles increased with the follicular development in control group,and remarkably in PCOS group. The average thickness of basal lamina of granulosa cells of primary follicles was 0.463±0.287μm in PCOS group and significantly thicker than 0.293±0.204μm in control group (P<0.05). The average thickness of basal lamina of granulosa cells of secondary follicles was 1.234±0.345μm in PCOS group and significantly thickened than 0.542±0.298μm in control group (P<0.01). The ultrastructure of granulosa cell of primordial follicle had no difference between two groups. The ultrastructure of granulosa cells in PCOS patients was obviously different from normal follicles with the follicular development. More abundant rough endoplasmic reticulum,free ribosome,well-developed Golgi body and lamellar mitochondrial crista,even abnormal-shape organelles can be found in granulosa cells PCOS group. The granulosa cells of pre-sinusoid follicles in control group had differentiation tendency while no such evidence was found in PCOS group. It is suggested that the thickness of basal lamina of granulose cells of the follicles may lead to decrease the permeability of FSH into follicles, resulting in hypofunction of FSH-granulosa cell axis and abnormal differentiation of granulosa cells.