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新生期胸腺切除通常所诱导的卵巢发育不全可通过预先给予雌激素来预防。

The ovarian dysgenesis normally induced by neonatal thymectomy is prevented by the prior administration of estrogen.

作者信息

Chapman J C, Griffin W J, Vassalo M F, Michael S D

机构信息

Department of Biological Sciences, State University of New York, Binghamton 13902-6000, USA.

出版信息

Am J Reprod Immunol. 1995 Sep;34(3):195-9. doi: 10.1111/j.1600-0897.1995.tb00938.x.

Abstract

PROBLEM

Neonatal thymectomy (Tx) and estrogen (E2) administration disrupt the reproductive and immune systems of female mice. The current experiment examined the combined effects of the two procedures on ovarian function, performed in sequence, and in reverse sequence.

METHOD

Groups of (C57BL/6J x A/J)F1 (B6A) female mice were given four daily injections of 20 micrograms estradiol-17 beta, either from 0 days to 3 days, or from 3 days to 6 days postpartum. In some groups this regimen was combined with thymectomy performed either prior to steroid injection (TX-3), or after steroid treatment (TX-4). Animals were sacrificed between 100 and 110 days of age then ovaries evaluated via light microscopy for dysgenesis and follicular cysts.

RESULTS

When E2 treatment followed Tx, the incidence of ovarian dysgenesis was unchanged (study 1, Tx + E2 = 60% ovarian dysgenesis; Tx = 63% ovarian dysgenesis) (study 2, Tx + E2 = 46% ovarian dysgenesis; Tx = 45% ovarian dysgenesis). In contrast, when E2 was given before Tx, ovarian dysgenesis did not occur (study 2, E2 + Tx = 0% ovarian dysgenesis; Tx = 46% ovarian dysgenesis). Ovaries from E2 + Tx animals were characteristic of ovaries from E2-injected animals without Tx.

CONCLUSION

The results indicate that E2 injection prevents Tx-induced ovarian dysgenesis, suggesting E2-activation of an extrathymic pathway for thymus function.

摘要

问题

新生小鼠胸腺切除术(Tx)和雌激素(E2)给药会破坏雌性小鼠的生殖和免疫系统。当前实验研究了这两种操作按顺序和逆序进行时对卵巢功能的联合影响。

方法

将(C57BL/6J×A/J)F1(B6A)雌性小鼠分为几组,在产后0天至3天或3天至6天每天注射4次20微克的17β-雌二醇。在一些组中,该方案与在类固醇注射前(TX-3)或类固醇治疗后(TX-4)进行的胸腺切除术相结合。在动物100至110日龄时处死,然后通过光学显微镜评估卵巢是否存在发育异常和卵泡囊肿。

结果

当E2治疗在Tx之后时,卵巢发育异常的发生率没有变化(研究1,Tx + E2 = 60%卵巢发育异常;Tx = 63%卵巢发育异常)(研究2,Tx + E2 = 46%卵巢发育异常;Tx = 45%卵巢发育异常)。相比之下,当E2在Tx之前给药时,未发生卵巢发育异常(研究2,E2 + Tx = 0%卵巢发育异常;Tx = 46%卵巢发育异常)。E2 + Tx动物的卵巢具有未进行Tx的E2注射动物卵巢的特征。

结论

结果表明E2注射可预防Tx诱导的卵巢发育异常,提示E2激活了胸腺外的胸腺功能途径。

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