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17β-雌二醇和环境雌激素4-壬基酚对凡纳滨对虾眼柄中促性腺抑制激素(GIH)表达的体内和体外抑制作用。

In vivo and in vitro inhibitory action of 17β-estradiol and environmental estrogen 4-nonylphenol on gonad-inhibiting hormone (GIH) expression in the eyestalks of Litopenaeus vannamei.

作者信息

Li G L, Chen H P, Deng S P, Ye M, Jiang S, Chan S F, Zhu C H

机构信息

Key Laboratory of Aquaculture in South China Sea for Aquatic Economic Animal of Guangdong Higher Education Institutes, Fisheries College, Guangdong Ocean University, Zhanjiang, China.

出版信息

Genet Mol Res. 2015 Oct 30;14(4):14056-65. doi: 10.4238/2015.October.29.25.

Abstract

The gonad-inhibiting hormone (GIH) belongs to a neuropeptide family synthesized and released in an X-organ sinus gland complex of crustacean eyestalks. GIH inhibits crustacean ovarian maturation by suppressing vitellogenin (Vtg) synthesis, whereas estrogen is responsible for the stimulation of vitellogenesis (not established). In this study, the effects of 17β-estradiol (E2, 10(-6) M), estrogen receptor antagonist tamoxifen (TAM, 10(-6), 10(-7), and 10(-8) M), and the environmental estrogen nonylphenol (NP, 1 μg/L and 100 μg/L) on LvGIH expression in the eyestalks of shrimp were determined by quantitative real-time PCR. Results showed that LvGIH expression decreased significantly during the L. vannamei ovarian maturation cycle. E2 and NP significantly reduced LvGIH transcripts in vivo, but TAM neutralized the inhibitory action of E2 in a dose-dependent manner (P < 0.05). In addition, the LvGIH expression levels decreased significantly in a time-dependent manner (P < 0.05) when ovary fragments were cultured in vitro with E2. The results of this study suggested that estrogen regulates GIH expression in L. vannamei eyestalks. E2 promoted ovarian development not only by directly upregulating vitellogenesis in the hepatopancreas, but it was also capable of downregulating LvGIH expression, which indirectly resulted in the stimulation of L. vannamei vitellogenesis.

摘要

促性腺抑制激素(GIH)属于一种神经肽家族,在甲壳类动物眼柄的X器官窦腺复合体中合成并释放。GIH通过抑制卵黄蛋白原(Vtg)的合成来抑制甲壳类动物卵巢成熟,而雌激素则负责刺激卵黄发生(尚未确定)。在本研究中,通过定量实时PCR测定了17β-雌二醇(E2,10⁻⁶ M)、雌激素受体拮抗剂他莫昔芬(TAM,10⁻⁶、10⁻⁷和10⁻⁸ M)以及环境雌激素壬基酚(NP,1 μg/L和100 μg/L)对虾眼柄中LvGIH表达的影响。结果表明,在凡纳滨对虾卵巢成熟周期中,LvGIH表达显著下降。E2和NP在体内显著降低了LvGIH转录本,但TAM以剂量依赖的方式中和了E2的抑制作用(P < 0.05)。此外,当卵巢片段与E2在体外培养时,LvGIH表达水平以时间依赖的方式显著下降(P < 0.05)。本研究结果表明,雌激素调节凡纳滨对虾眼柄中GIH的表达。E2不仅通过直接上调肝胰腺中的卵黄发生来促进卵巢发育,还能够下调LvGIH表达,从而间接刺激凡纳滨对虾的卵黄发生。

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