Molecular mechanism of ovarian toxicity of Hook.F. a study based on network pharmacology and molecular docking / 浙江大学学报·医学版

To explore the mechanism of ovarian toxicity of Hook. F. (TwHF) by network pharmacology and molecular docking. The candidate toxic compounds and targets of TwHF were collected by the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) and the Comparative Toxicogenomics Database (CTD). Then, the potential ovarian toxic targets were obtained from CTD, and the target genes of ovarian toxicity of TwHF were analyzed using the STRING database. The protein-protein interaction (PPI) network was established by Cytoscape and analyzed by the cytoHubba plug-in to identify hub genes. Additionally, the target genes of ovarian toxicity of TwHF were subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses by using the R software. Finally, Discovery Studio software was used for molecular docking verification of the core toxic compounds and the hub genes. Nine candidate toxic compounds of TwHF and 56 potential ovarian toxic targets were identified in this study. Further network analysis showed that the core ovarian toxic compounds of TwHF were triptolide, kaempferol and tripterine, and the hub ovarian toxic genes included , , , , , , , , and . Besides, the GO and KEGG analysis indicated that TwHF caused ovarian toxicity through oxidative stress, reproductive system development and function, regulation of cell cycle, response to endogenous hormones and exogenous stimuli, apoptosis regulation and aging. The docking studies suggested that 3 core ovarian toxic compounds of TwHF were able to fit in the binding pocket of the 10 hub genes. TwHF may cause ovarian toxicity by acting on 10 hub genes and 140 signaling pathways.

Study of the prevention of carboplation-induced reproduction damage by gonadotropin-releasing hormone agonist / 中国综合临床

Objective To study the effect of gonadotropin releasing hormone agonist(GnRHa)against car-boplation-induced gonadotoxicity in rats. Methods Forty Wistar rats were divided into four groups which received carboplation, GnRHa + carboplation, GnRHa and normal saline respectively(n=10 for each group). Blood samples were collected from the abdominal aorta and the levels of blood follicle stimulation hormone (FSH) and estradiol (E<2>) were determined. Both ovaries and uterus of each rat were removed to measure the amount and the maturity of follicles. Body mass and morphological and pathological features of the rats were also observed. Results Compared with that in control group, the body mass of ovary and uterus decreased (P<0.05), and a significant reduction was observed in the number of ovarian follicles at each grade (P<0.05). The levels of E2 significantly lowered (P<0.05) and the level of FSH markedly ascended in group carboplation. Compared with that in group carboplation, the amount of primitive follicles significantly increased in group GnRHa + carboplation (P<0.05), and carboplation showed markedly protective effect on the ovarian and uterine morphological construction of rats. Conclusion Gn-Rha, appliying to preventing the rat reproduction damage in advance, has the certain protective function.