Guo Qin, Gao Rui-Ping, Tao Ying
Department of Gynaecology and Obstetrics, the First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou 510080, China.
Sichuan Da Xue Xue Bao Yi Xue Ban. 2020 Nov;51(6):817-821. doi: 10.12182/20200960603.
To investigate the expression of peroxisome proliferator-activated receptor γ co-activator 1α (PGC-1α) in the ovarian tissue of polycystic ovary syndrome (PCOS) rat model and obese PCOS rat model, and the possible mechanism of PCOS.
Thirty SD rats were randomly divided into control group, PCOS rat model group and obese PCOS rat model group. DHEA dissolved in 0.2 mL soybean oil was injected daily into the rats of two PCOS groups for 21 d. Rats in obese PCOS model group were added with high-fat diet based on DHEA modeling, and each group had 10 rats. Body mass were measured before and on the 22 day after modeling. The serum testosterone (T) levels were measured by abdominal aortic blood, and the ovarian tissues of rats were taken for histological changes were observed by HE staining, immunohistochemical staining and Western blot to detect PGC-1ɑ protein expression.
The body mass of rats in each group increased after modeling, and the body mass of rats in PCOS group and obese PCOS group increased significantly ( <0.05). The serum T concentration of two PCOS model groups was higher than that of control group ( <0.01). The serum T concentration in obese PCOS model group was higher than that in the PCOS group ( <0.05). The results of HE staining of rat ovarian tissue showed that there were follicles and a small amount of corpus luteum at different developmental stages in the control group, and the granulosa cells were arranged in 4-6 layers. The number of immature small follicles in the two PCOS groups was significantly increased. The granulosa cells were arranged in 1-3 layers, relatively looser, and some follicles were atresia. In the obese PCOS group, the diameter of ovarian atretic follicles increased, the number of granulocyte layers decreased, and oocytes disappeared more obviously. Immunohistochemical staining showed that the PGC-1ɑ protein was mainly expressed in the cumulus and granulosa cells of ovarian tissue in the control group. The mean gray level of PGC-1ɑ protein expression in PCOS group (0.53±0.06) and obese PCOS group (0.36±0.03) was lower than that of the control group (0.75±0.03), with the statistical difference ( <0.05). PGC-1ɑ expression in the obese PCOS group was lower than that in the PCOS group ( <0.01). The results of Western blot were consistent with those of immunohistochemical staining.
PGC-1ɑ is associated with damage of ovarian granulosa cells in high-fat environment. The decrease of PGC-1ɑ expression in granulosa cells of ovarian follicles may be an important cause of PCOS development.
探讨过氧化物酶体增殖物激活受体γ共激活因子1α（PGC-1α）在多囊卵巢综合征（PCOS）大鼠模型及肥胖PCOS大鼠模型卵巢组织中的表达情况及PCOS可能的发病机制。
将30只SD大鼠随机分为对照组、PCOS大鼠模型组和肥胖PCOS大鼠模型组。对两个PCOS组的大鼠每日腹腔注射溶解于0.2 mL大豆油中的脱氢表雄酮（DHEA），连续注射21 d。肥胖PCOS模型组大鼠在DHEA造模基础上给予高脂饮食，每组10只大鼠。在造模前及造模后第22天测量大鼠体质量。经腹主动脉取血测定血清睾酮（T）水平，取大鼠卵巢组织进行HE染色观察组织学变化，采用免疫组织化学染色及蛋白质免疫印迹法检测PGC-1α蛋白表达。
造模后各组大鼠体质量均增加，PCOS组和肥胖PCOS组大鼠体质量增加显著（P<0.05）。两个PCOS模型组血清T浓度均高于对照组（P<0.01）。肥胖PCOS模型组血清T浓度高于PCOS组（P<0.05）。大鼠卵巢组织HE染色结果显示，对照组卵巢有不同发育阶段的卵泡及少量黄体，颗粒细胞排列为46层。两个PCOS组未成熟小卵泡数量显著增加，颗粒细胞排列为13层，较为疏松，部分卵泡闭锁。肥胖PCOS组卵巢闭锁卵泡直径增大，颗粒细胞层数减少，卵母细胞消失更明显。免疫组织化学染色显示，对照组卵巢组织中PGC-1α蛋白主要表达于卵丘及颗粒细胞。PCOS组（0.53±0.06）和肥胖PCOS组（0.36±0.03）PGC-1α蛋白表达的平均灰度值低于对照组（0.75±0.03），差异有统计学意义（P<0.05）。肥胖PCOS组PGC-1α表达低于PCOS组（P<0.01）。蛋白质免疫印迹法结果与免疫组织化学染色结果一致。
PGC-1α与高脂环境下卵巢颗粒细胞损伤有关。卵巢卵泡颗粒细胞中PGC-1α表达降低可能是PCOS发生发展的重要原因。
