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Biological mechanisms of premature ovarian failure caused by psychological stress based on support vector regression

机译:基于支持向量回归的心理应激导致卵巢早衰的生物学机制

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摘要

Psychological stress has become a common and important cause of premature ovarian failure (POF). Therefore, it is very important to explore the mechanisms of POF resulting from psychological stress. Sixty SD rats were randomly divided into control and model groups. Biomolecules associated with POF (β-EP, IL-1, NOS, NO, GnRH, CRH, FSH, LH, E2, P, ACTH, and CORT) were measured in the control and psychologically stressed rats. The regulation relationships of the biomolecules were explored in the psychologically stressed state using support vector regression (SVR). The values of β-EP, IL-1, NOS, and GnRH in the hypothalamus decreased significantly, and the value of NO changed slightly, when the values of 3 biomolecules in the hypothalamic-pituitary-adrenal axis decreased. The values of E2 and P in the hypothalamic-pituitary-ovarian axis decreased significantly, while the values of FSH and LH changed slightly, when the values of the biomolecules in the hypothalamus decreased. The values of FSH and LH in the pituitary layer of the hypothalamic-pituitary-ovarian axis changed slightly when the values of E2 and P in the target gland layer of the hypothalamic-pituitary-ovarian axis decreased. An Imbalance in the neuroendocrine-immune bimolecular network, particularly the failure of the feedback action of the target gland layer to pituitary layer in the pituitary-ovarian axis, is possibly one of the pathogenic mechanisms of POF.
机译:心理压力已成为卵巢早衰(POF)的常见且重要原因。因此,探索心理压力导致POF的机制非常重要。 60只SD大鼠随机分为对照组和模型组。在对照组和有心理压力的大鼠中测量了与POF相关的生物分子(β-EP,IL-1,NOS,NO,GnRH,CRH,FSH,LH,E2,P,ACTH和CORT)。使用支持向量回归(SVR)探索了在心理压力状态下生物分子的调节关系。当下丘脑-垂体-肾上腺轴中的3种生物分子的值降低时,下丘脑中的β-EP,IL-1,NOS和GnRH的值显着降低,NO的值略有变化。下丘脑-垂体-卵巢轴上的E2和P值显着下降,而当下丘脑中的生物分子值下降时,FSH和LH值则略有变化。当下丘脑-垂体-卵巢轴的目标腺体中的E2和P值降低时,下丘脑-垂体-卵巢轴的垂体层中的FSH和LH值略有变化。神经内分泌免疫双分子网络的失衡,特别是靶腺层对垂体-卵巢轴对垂体层的反馈作用的失败,可能是POF的致病机制之一。

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