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Biochemical and histological evidence of thyroid gland dysfunction in estradiol valerate model of the polycystic ovary in Wistar rats

机译:Wistar大鼠雌激素卵巢雌激素卵巢模型中甲状腺腺体功能障碍的生化和组织学

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Thyroid defects and polycystic ovary (PSO) disease are prevalent endocrine problems among humans. While various studies investigated the ovarian function and histological alterations during estradiol valerate model of PCO, yet, there were no available studies examining thyroid gland function and histology. Therefore, the present study aimed to investigate linkage between estradiol valerate-induced PCO and the development of thyroid dysfunction in rats. The study comprises 2 groups of male Wistar rats (n = 12), control group and PCO group. PCO was induced by injecting two doses of estradiol valerate with 6 weeks lag period in between. After twelve weeks, PCO was confirmed by vaginal smear examination which showed marked vaginal cornification. In addition, the light microscopic examination of the ovaries revealed chief histological signs of PCO like numerous cysts and damaged follicles. In addition, PCO induced rats showed decreased serum LH and increased serum FSH levels. Thyroid hypoactivity was confirmed by increased serum TSH and decreased serum thyroid hormones (T3, and T4). Histologically, the thyroid tissue revealed small-size follicles devoid of the colloid and increased connective tissue between follicles. Semithin sections showed hypertrophied and/or flat follicular cells as well as increased resorption colloidal granules. Ultrathin sections showed low height cells with dark nucleus and heterochromatin. Furthermore, PCO-induced rats thyroid gland tissue revealed increased expression of the apoptotic mediator caspase-3. There was also a decrease in the expression of proliferating cell nuclear antigen. In summary, this study provides several effective biochemical and histological evidences for thyroid gland dysfunction in PCO-induced rats. (C) 2019 Elsevier Inc. All rights reserved.
机译:甲状腺缺陷和多囊卵巢(PSO)疾病是人类中普遍的内分泌问题。虽然各种研究在PCO的雌二醇标度模型中调查了卵巢功能和组织学改变,但没有可用的研究检查甲状腺功能和组织学。因此,本研究旨在探讨雌二醇标度诱导的PCO之间的联系和大鼠甲状腺功能障碍的发育。该研究包括2组雄性Wistar大鼠(n = 12),对照组和PCO组。通过将两剂雌二醇符号注入其中的两剂溶于6周的滞后期,诱导PCO。十二周后,PCO通过阴道涂片检查证实,显示出显着的阴道弯曲。此外,卵巢的光学显微镜检查揭示了PCO的主要组织学标志,如许多囊肿和损坏的卵泡。此外,PCO诱导的大鼠显示出降低的血清LH和血清FSH水平增加。通过增加的血清TSH和降低的血清甲状腺激素(T3和T4)来确认甲状腺脱乳性。组织学上,甲状腺组织揭示了小尺寸的卵泡,卵泡之间的胶体和增加的结缔组织。半素部分显示出嗜肥和/或扁平卵泡细胞以及增加的吸收胶体颗粒。超薄部分显示出低高度细胞,具有深色细胞核和异铬胺。此外,PCO诱导的大鼠甲状腺组织揭示了凋亡介质Caspase-3的表达增加。增殖细胞核抗原的表达也有降低。总之,本研究为PCO诱导的大鼠中的甲状腺功能障碍提供了几种有效的生化和组织学证据。 (c)2019 Elsevier Inc.保留所有权利。

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