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首页> 外文期刊>Histology and histopathology >Thyroxine treatment stimulated ovarian follicular angiogenesis in immature hypothyroid rats.
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Thyroxine treatment stimulated ovarian follicular angiogenesis in immature hypothyroid rats.

机译:甲状腺素治疗可刺激未成熟甲状腺功能减退大鼠的卵泡血管生成。

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摘要

The development of mature ovarian follicles is greatly dependent on healthy thecal angiogenesis. Recent experimental evidence showed that thyroxine (T4) treatment promoted ovarian follicle development in immature hypothyroid (rdw) rats. However, an involvement of thyroid hormone in ovarian follicular angiogenesis has not yet been demonstrated. By morphological and molecular approaches, the present studies demonstrated that antral follicles in untreated, T4- or equine chorionic gonadotropin (eCG)-treated rdw rats were mainly small and/or atretic, and presented a poorly developed thecal microvasculature with ultrastructural evidence of diffuse quiescent or degenerative thin capillaries. However, T4 together with eCG increased the number of large antral and mature follicles with numerous activated capillaries and ultra-structural evidence of rich and diffuse angiogenesis in the theca layer. While T4 alone significantly increased mRNA expression of vascular endothelial growth factor (VEGF) and tumor necrosis factor alpha (TNFalpha), it decreased that of fetal liver kinase compared with those in the untreated group. Combined treatment of T4 and eCG markedly increased mRNA abundance of not only VEGF and TNFalpha, but also basic fibroblast growth factor. These data suggest that T4 may promote ovarian follicular angiogenesis in rdw rats by up-regulating mRNA expression of major angiogenic factors.
机译:成熟的卵巢卵泡的发育在很大程度上取决于健康的鞘内血管生成。最近的实验证据表明,甲状腺素(T4)处理可促进未成熟甲状腺功能减退(rdw)大鼠的卵巢卵泡发育。然而,尚未证实甲状腺激素参与卵巢滤泡性血管生成。通过形态学和分子方法,本研究表明,未经治疗的,T4或马绒毛膜促性腺激素(eCG)处理的rdw大鼠的窦房卵泡主要是小和/或闭锁的,并且其皮层微血管发育不良,具有弥散静止的超微结构证据或退化的细毛细管。然而,T4与eCG一起增加了具有大量活化毛细管的大型肛门和成熟卵泡的数量,并在卵泡膜层富集和弥漫性血管生成的超结构证据。尽管单独的T4显着增加了血管内皮生长因子(VEGF)和肿瘤坏死因子α(TNFalpha)的mRNA表达,但与未治疗组相比,它降低了胎儿肝激酶的mRNA表达。 T4和eCG的联合治疗不仅显着增加了VEGF和TNFalpha的mRNA丰度,还显着增加了碱性成纤维细胞生长因子的mRNA丰度。这些数据表明T4可能通过上调主要血管生成因子的mRNA表达来促进rdw大鼠卵巢滤泡性血管生成。

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