chrysin has been researched along with Primary-Ovarian-Insufficiency* in 2 studies
2 other study(ies) available for chrysin and Primary-Ovarian-Insufficiency
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Chrysin reduces inflammation and oxidative stress and improves ovarian function in D-gal-induced premature ovarian failure.
Premature ovarian failure (POF), a frequently occurring pathology. Chrysin has antioxidant, anti-inflammatory, anti-apoptotic and other pharmacological activities. This study was designed to detect the effect of Chrysin on POF. The establishment of POF was depended on the subcutaneous injection of D-gal (200 mg/kg/d). With the adoption of ELISA, the levels of hormones and release of inflammatory cytokines were assayed. The expression of MDA, GSH-px, SOD and ROS was evaluated with corresponding kits. In addition, the pathological changes of ovary and apoptosis of ovarian granulosa cells in D-gal-induced mice were detected using H&E staining and TUNEL, respectively. Moreover, the levels of FSH receptor and apoptosis-related proteins were measured with western blot. Finally, ERβ expression was measured with RT-qPCR and western blot. In this study, we found that chrysin regulated the expression of hormones and weight of D-gal-induced mice. It was also found that chrysin inhibited the inflammation and oxidative stress in mice with D-gal induction. In addition, the number and advancement of follicle in D-gal-induced mice treated with chrysin revealed that chrysin could improve the ovarian function of mice with POF. Furthermore, chrysin exhibited inhibitory effects on the apoptosis of ovarian granulosa cells in D-gal-induced mice. More importantly, chrysin molecule targeted ERβ and activated ERβ expression in POF. Overall, Chrysin reduces inflammation and oxidative stress and improves ovarian function in D-gal-induced premature ovarian failure, suggesting that chrysin is valuable for the treatment of POF. Topics: Animals; Apoptosis; Estrogen Receptor beta; Female; Flavonoids; Hormones; Humans; Inflammation; Mice; Mice, Inbred C57BL; Oxidative Stress; Primary Ovarian Insufficiency | 2022 |
Mechanistic approach of the inhibitory effect of chrysin on inflammatory and apoptotic events implicated in radiation-induced premature ovarian failure: Emphasis on TGF-β/MAPKs signaling pathway.
Radiotherapy is one of the most relevant treatment modalities for various types of malignancies. However, it causes premature ovarian failure (POF) and subsequent infertility in women of reproductive age; hence urging the development of effective radioprotective agents. Chrysin, a natural flavone, possesses several pharmacological activities owing to its antioxidant, anti-inflammatory and anti-apoptotic properties. Therefore, the aim of this study was to investigate the efficacy of chrysin in limiting γ-radiation-mediated POF and to elucidate the underlying molecular mechanisms. Immature female Sprague-Dawley rats were subjected to a single dose of γ-radiation (3.2 Gy) and/or treated with chrysin (50 mg/kg) once daily for two weeks before and three days post-irradiation. Chrysin prevented the radiation-induced ovarian dysfunction by restoring estradiol levels, preserving the normal ovarian histoarchitecture and combating the follicular loss. Eelectron microscopic analysis showed that the disruption of ultrastructure components due to radiation exposure was hampered by chrysin administration. Mechanistically, chrsyin was able to reduce the levels of the inflammatory markers NF-κB, TNF-α, iNOS and COX-2 in radiation-induced ovarian damage. Chrysin also exhibited potent anti-apoptotic effects against radiation-induced cell death by downregulating the expression of cytochrome c and caspase 3. Radiation obviously induced upregulation of TGF-β protein with subsequent phospholyration and hence activation of downstream mitogen-activated protein kinases (MAPKs); p38 and JNK. Notably, administration of chrysin successfully counteracted these effects. These findings revealed that chrysin may be beneficial in ameliorating radiation-induced POF, predominantly via downregulating TGF-β/MAPK signaling pathways leading subsequently to hindering inflammatory and apoptotic signal transduction pathways implicated in POF. Topics: Animals; Apoptosis; Cytoprotection; Female; Flavonoids; Inflammation Mediators; MAP Kinase Signaling System; Primary Ovarian Insufficiency; Radiation Injuries, Experimental; Rats; Rats, Sprague-Dawley; Signal Transduction; Transforming Growth Factor beta; Treatment Outcome | 2019 |