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目的:研究不同剂量凋膜止崩液对雌激素负荷去势大鼠孕激素(P)及其受体(PR)的影响,揭示药物在有效部位靶向干预条件下,HPOA(下丘脑-垂体-卵巢轴)调节通道靶端药物效应机制,探讨靶向药物治疗功能失调性子宫出血(DUB)的分子生物学机制。方法:将大鼠随机分为4组:空白组(A)、模型组(B)、凋膜止崩液小剂量组(C)、凋膜止崩液大剂量组(D),采用雌激素负荷去势法建立大鼠增生过长子宫内膜动物模型,放射免疫法测定各组大鼠血清孕激素(P)水平,免疫组织化学染色观察大鼠子宫内膜细胞孕激素受体(PR)的表达。结果:血清中P的水平:B组与C组相比有显著性差异(P<0.01),C组与D组之间比较无统计学意义(P>0.05);子宫内膜PR的表达:C组、D组子宫内膜PR表达明显降低,与B组相比有显著统计学差异(P<0.01);C组与D组之间无明显统计学差异(P>0.05)。结论:凋膜止崩液可能通过直接或间接的作用调节P、PR消除增生过长子宫内膜。
Objective: To study the effect of different doses of Dipsacus decoction on progesterone (P) and its receptor (PR) in estrogen-loaded castrated rats, and to reveal that HPOA (hypothalamus-pituitary - Ovarian Axis) regulates the drug effect mechanism at the target end of the channel and explores the molecular biological mechanism of targeted drug therapy for dysfunctional uterine bleeding (DUB). Methods: The rats were randomly divided into 4 groups: the blank group (A), the model group (B), the low dose group of Cunninghamia campestris (C) and the high dose group of Danshiganlung decoction (D) The animal model of hyperplasia of endometrium was established by the method of load-shedding. The level of progesterone (P) in rat serum was determined by radioimmunoassay. The levels of progesterone receptor (PR) expression. Results: The level of P in serum: There was significant difference between group B and group C (P <0.01), but there was no significant difference between group C and group D (P> 0.05). The expression of PR in endometrium: The expression of PR in C group and D group was significantly lower than that in B group (P <0.01). There was no significant difference between C group and D group (P> 0.05). Conclusion: Dingsidengruanbian may regulate P and PR directly or indirectly to eliminate hyperproliferative endometrium.