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目的:探讨正常及心理应激状态下影响卵巢早衰的各生物分子之间相互调控关系。方法:SD大鼠60只,随机分为两组:正常组和模型组;分别检测其正常及心理应激状态下与卵巢早衰相关的生物分子:β-EP、IL-1、NOS、NO、ER、PR、GnRH、CRH、FSH、LH、E2、P、ACTH和CORT;利用因子分析方法探究正常及心理应激状态各生物分子之间的相互调控关系,并探寻心理应激导致卵巢早衰过程中的关键生物分子。结果:正常状态主调控因子主要包括下丘脑生物分子和垂体-卵巢轴生物分子;心理应激状态下主调控因子包括垂体-肾上腺轴生物分子ACTH及下丘脑和垂体-卵巢轴生物分子,且IL-1是心理应激状态第1和第2公共因子上共有的下丘脑部位的生物分子。结论:正常状态下丘脑生物分子与垂体-卵巢轴生物分子之间关系密切,垂体-肾上腺轴生物分子相对独立;而心理应激状态主调控关系显示了垂体-肾上腺轴上的生物分子ACTH对下丘脑和垂体-卵巢轴生物分子的反馈影响,初步揭示了心理应激首先引起垂体-肾上腺轴生物分子变化,进而通过下丘脑生物分子IL-1使下丘脑-垂体-卵巢轴紊乱,导致卵巢早衰的生物学机制。
OBJECTIVE: To investigate the mutual regulation of various biomolecules that affect premature ovarian failure in normal and psychological stress states. Methods: Sixty SD rats were randomly divided into two groups: normal group and model group. The levels of β-EP, IL-1, NOS, ER, PR, GnRH, CRH, FSH, LH, E2, P, ACTH and CORT. The relationship between normal and psychological states of biomolecules was explored by means of factor analysis, and the psychological stress induced the process of premature ovarian failure In the key biomolecules. Results: The main regulators of normal state included hypothalamic biomolecules and pituitary-ovarian axis biomolecules. Under psychological stress, the main regulators included ACTH of hypothalamic-pituitary-ovarian axis and biomolecules of hypothalamus and pituitary-ovarian axis, and IL -1 is the biomolecule of the hypothalamus common to the first and second common factors of psychic stress. Conclusion: Under normal conditions, the biological molecules of the hypothalamus are closely related to the biological molecules of the pituitary-ovarian axis, while the biological molecules of the pituitary-adrenal axis are relatively independent. The main regulatory relationship of the psychological stress states shows that the biotinylation of ACTH on the pituitary-adrenal axis Hypothalamic-pituitary-ovarian axis biomolecules, and initially revealed that psychological stress firstly caused the changes of the biomolecules in the pituitary-adrenal axis and then disturbed the hypothalamus-pituitary-ovarian axis through the hypothalamic biomolecule IL-1, leading to premature ovarian failure Biological mechanism.