Prolactin and lipopolysaccharide treatment increased apoptosis and atresia in rat ovarian follicles

Prolactin and lipopolysaccharide treatment increased apoptosis and atresia in rat ovarian follicles
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DOI:
10.1046/j.1365-201x.2001.00813.x
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发表时间:
2001-05-01
期刊:
ACTA PHYSIOLOGICA SCANDINAVICA
影响因子:
--
通讯作者:
Whitehead, SA
Whitehead, SA
中科院分区:
其他
文献类型:
--
作者:
Besnard, N;Horne, EAL;Whitehead, SA

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滤泡闭锁与滤泡内巨噬细胞增多有关。目前尚不清楚的是,在成年大鼠中,巨噬细胞是否有助于诱导细胞凋亡和/或闭锁,或者它们是否仅仅是激素介导事件的继发。由于催乳素是一种免疫反应性激素,可刺激单核细胞趋化因子的表达,本实验比较了催乳素处理与脂多糖(LPS)免疫刺激对巨噬细胞侵入卵巢卵泡和黄体隔室的影响,以及巨噬细胞入侵相关的凋亡/闭锁的发生。大鼠分别用催乳素或LPS治疗3天,分别在发情前或发情时获得卵巢。催乳素和脂多糖增加了发潮前卵巢闭锁卵泡数量(P < 0.008,(2)),增加了凋亡细胞和巨噬细胞的平均数量(部分组P < 0.05)。巨噬细胞多见于鞘层,凋亡细胞多见于颗粒细胞层,但颗粒细胞层内有巨噬细胞的滤泡中有84%含有较多的凋亡核。体内催乳素和LPS处理降低了卵巢分散体培养中黄体酮对促卵泡激素(FSH)的反应(P < 0.001),但没有抑制对福斯克林的反应。相反,体外添加催乳素或脂多糖抑制孕酮对福斯克林的反应。结果表明,催乳素和脂多糖均可增加卵泡凋亡和闭锁,降低孕激素对卵泡刺激素的反应。
Follicular atresia is associated with the presence of increased macrophages within the follicle. What is not known is whether, in the adult rat, macrophages are instrumental in inducing apoptosis and/or atresia or whether they are simply secondary to a hormonally mediated event. As prolactin is an immunoreactive hormone and stimulates the expression of monocyte chemoattractant, the present experiments compared the effects of prolactin treatment with that of an immune challenge with lipopolysaccharide (LPS) on the invasion of macrophages into the follicular and luteal compartments of the ovary and the occurrence of apoptosis/atresia in relation to macrophage invasion. Rats were treated for 3 days with either prolactin or LPS and ovaries obtained at pro-oestrus or oestrus. Prolactin and LPS increased the number of atretic vs. healthy follicles (P < 0.008, (2)) in pro-oestrus ovaries and increased the mean number of apoptotic cells and macrophages (P < 0.05 for some groups). Macrophages were typically observed in the thecal layer, apoptotic cells in the granulosa cell layer, although 84% follicles which had macrophages within the granulosa cell layer also contained relatively high numbers of apoptotic nuclei. Prolactin and LPS treatment in vivo reduced the progesterone response to follicle stimulating hormone (FSH) (P < 0.001) in cultures of ovarian dispersates but did not inhibit the response to forskolin. In contrast, prolactin or LPS added in vitro to the cultures inhibited the progesterone response to forskolin. Results shaw that both prolactin and LPS increase follicular apoptosis and atresia and reduce the progesterone response to FSH.