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三苯基氯化锡诱导大鼠着床失败的原因:子宫蜕膜化的抑制

Suppression of uterine decidualization as a cause of implantation failure induced by triphenyltin chloride in rats.

作者信息

Ema M, Miyawaki E, Kawashima K

机构信息

National Institute of Health Sciences, Osaka Branch, Japan.

出版信息

Arch Toxicol. 1999 Apr-May;73(3):175-9. doi: 10.1007/s002040050603.

DOI:10.1007/s002040050603
PMID:10401684
Abstract

In our previous study, triphenyltin chloride (TPTC1) was found to induce implantation failure, as preimplantation embryonic loss, in rats. In this study, the effects of TPTC1 on the uterine function, as a cause of implantation failure, were determined using pseudopregnant rats. Female rats were given TPTC1 by gastric intubation at 3.1, 4.7, and 6.3 mg/kg on pseudopregnant day (PPD) 0 to PPD 3 and the decidual cell response was induced on PPD 4. The uterine weight on PPD 9 served as an index of uterine decidualization. A significant decrease in the uterine weight, which indicates suppression of the uterine decidualization, was detected at 4.7 and 6.3 mg/kg. In our previous study, these doses induced a significant increase in implantation failure in female rats given TPTC1 on gestational day (GD) 0 to 3. The ovarian weight and number of corpora lutea in the TPTC1-treated groups were comparable to that of the controls. A significant decrease in serum progesterone levels after administration of TPTC1 was found at 4.7 and 6.3 mg/kg. These findings suggest that implantation failure due to TPTC1 may be mediated via the suppression of uterine decidualization and correlated with the reduction in serum progesterone levels.

摘要

在我们之前的研究中,发现三苯基氯化锡(TPTC1)会导致大鼠出现着床失败,即着床前胚胎丢失。在本研究中,使用假孕大鼠确定了TPTC1对子宫功能(作为着床失败的一个原因)的影响。在假孕第(PPD)0至PPD 3天,给雌性大鼠经胃插管给予3.1、4.7和6.3 mg/kg的TPTC1,并在PPD 4天诱导蜕膜细胞反应。PPD 9天的子宫重量作为子宫蜕膜化的指标。在4.7和6.3 mg/kg剂量下,检测到子宫重量显著下降,这表明子宫蜕膜化受到抑制。在我们之前的研究中,这些剂量在妊娠第(GD)0至3天给予TPTC1的雌性大鼠中诱导着床失败显著增加。TPTC1处理组的卵巢重量和黄体数量与对照组相当。在4.7和6.3 mg/kg剂量下,发现给予TPTC1后血清孕酮水平显著下降。这些发现表明,TPTC1导致的着床失败可能是通过抑制子宫蜕膜化介导的,并且与血清孕酮水平降低相关。

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