Study summary · research use only
Kisspeptin-10 inhibits OHSS by suppressing VEGF secretion
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study examined effects of kisspeptin-10 (Kp-10) on ovarian hyperstimulation syndrome (OHSS) using OHSS rat models, human umbilical vein endothelial cells (HUVECs), and human luteinized granulosa cells. Decreased Kiss1r expression was observed in ovaries and lung tissue of OHSS rats. Injection of exogenous Kp-10 was associated with reduced vascular permeability (VP) and VEGF increases while promoting Kiss1r expression in ovarian and lung tissue of OHSS rats. In HUVECs, a high level of 17-beta estradiol (E2), a feature of OHSS, was associated with suppressed KISS1R expression and increased VEGF and nitric oxide (NO) through estrogen receptors (ESR2). KISS1R mRNA was also decreased in luteinized granulosa cells from high-risk OHSS human patients. The authors describe Kp-10 as limiting increased VP in OHSS through KISS1R activation and VEGF inhibition.
Abstract
The aim of the present study was to elucidate the effects of kisspeptin-10 (Kp-10) on ovarian hyperstimulation syndrome (OHSS) and its related mechanism in OHSS rat models, human umbilical vein endothelial cells (HUVECs) and human luteinized granulosa cells. OHSS is a systemic disorder with high vascular permeability (VP) and ovarian enlargement. KISS1R (KISS1 receptor) is the specific receptor of kisspeptin. The kisspeptin/KISS1R system inhibits the expression of vascular endothelial growth factor (VEGF), which is the main regulator of VP. In our study, decreased expression of Kiss1r was observed in both ovaries and lung tissue of OHSS rats. Injection of exogenous Kp-10 inhibited the increase of VP and VEGF while promoting the expression of Kiss1r in both the ovarian and lung tissue of OHSS rats. Using HUVECs, we revealed that a high level of 17-β estradiol (E2), a feature of OHSS, suppressed the expression of KISS1R and increased VEGF and nitric oxide (NO) through estrogen receptors (ESR2). Furthermore, KISS1R mRNA also decreased in the luteinized human granulosa cells of high-risk OHSS patients, and was consistent with the results in rat models and HUVECs. In conclusion, Kp-10 prevents the increased VP of OHSS by the activation of KISS1R and the inhibition of VEGF.
pepmg summarizes the peer-reviewed literature and links to every source — it sells nothing, ships nothing, and gives no medical, dosing, or human-use guidance. Don't just trust this summary: follow the citation to its source and read it yourself. Research use only.