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内脂素蛋白可能是导致幼鼠卵巢增殖抑制和细胞凋亡的原因。

Visfatin protein may be responsible for suppression of proliferation and apoptosis in the infantile mice ovary.

作者信息

Annie Lalrawngbawli, Gurusubramanian Guruswami, Kumar Roy Vikas

机构信息

Department of Zoology, Mizoram University, Aizawl, Mizoram - 796 004, India.

Department of Zoology, Mizoram University, Aizawl, Mizoram - 796 004, India.

出版信息

Cytokine. 2021 Apr;140:155422. doi: 10.1016/j.cyto.2021.155422. Epub 2021 Jan 18.

DOI:10.1016/j.cyto.2021.155422
PMID:33476980
Abstract

Visfatin is an important adipokines, which are expressed in different tissues including ovary of mammals. The postnatal ovary in rodents undergoes dramatic changes of intra-ovarian factors in relation to proliferation and apoptosis. There are studies which showed that gonadal visfatin changes in postnatal life. However, role of visfatin in the early postnatal period i.e. infantile period has not been studied. Therefore, the present study was aimed to explore the role of visfatin in the early postnatal ovarian functions. Furthermore, to explore the role of visfatin, the endogenous visfatin was inhibited from PND14-PND21 by FK866 with dose of 1.5 mg/kg. Our results showed gain in body weight and ovarian weight after visfatin inhibition. The inhibition of visfatin increased the ovarian proliferation (increase in PCNA, GCNA expression and BrdU incorporation) and apoptosis (increase in BAX and active caspase3 expression). Moreover, visfatin inhibition decreased the expression of antiapoptotic/survival protein, BCL2 in the ovary. These findings suggest that visfatin in the infantile ovary may suppress the proliferation and apoptosis by up-regulating BCL2 expression. An interesting finding has been observed that circulating estrogen and progesterone remain unaffected, although visfatin inhibition up-regulated ER-β and down-regulated ER-α. It may also be suggested that visfatin could regulates proliferation and apoptosis via modulating estrogen signaling. In conclusion, visfatin inhibits the proliferation and apoptosis without modulating the ovarian steroid biosynthesis and visfatin mediated BCL2 expression could also be mechanism to preserve the good quality follicle in early postnatal period.

摘要

内脂素是一种重要的脂肪因子,在包括哺乳动物卵巢在内的不同组织中表达。啮齿动物出生后的卵巢会经历与增殖和凋亡相关的卵巢内因子的剧烈变化。有研究表明,性腺内脂素在出生后的生命过程中会发生变化。然而,内脂素在出生后早期即婴儿期的作用尚未得到研究。因此,本研究旨在探讨内脂素在出生后早期卵巢功能中的作用。此外,为了探究内脂素的作用,在出生后第14天至第21天,用剂量为1.5毫克/千克的FK866抑制内源性内脂素。我们的结果显示,抑制内脂素后体重和卵巢重量增加。抑制内脂素可增加卵巢增殖(增殖细胞核抗原、生殖细胞细胞核抗原表达增加以及5-溴脱氧尿嘧啶核苷掺入增加)和凋亡(促凋亡蛋白BAX和活化的半胱天冬酶3表达增加)。此外,抑制内脂素可降低卵巢中抗凋亡/存活蛋白BCL2的表达。这些发现表明,婴儿期卵巢中的内脂素可能通过上调BCL2表达来抑制增殖和凋亡。一个有趣的发现是,尽管抑制内脂素会上调雌激素受体β并下调雌激素受体α,但循环中的雌激素和孕酮仍未受影响。也可以认为,内脂素可能通过调节雌激素信号来调节增殖和凋亡。总之,内脂素抑制增殖和凋亡而不调节卵巢类固醇生物合成,内脂素介导的BCL2表达也可能是在出生后早期维持优质卵泡的机制。

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