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Novel Molecular Mechanisms Underlying the Ameliorative Effect of Platelet-Rich Plasma against Electron Radiation-Induced Premature Ovarian Failure

炎症 卵巢早衰 细胞凋亡 内科学 内分泌学 细胞因子 医学 血小板 癌症研究 男科 免疫学 化学 生物化学
作者
Grigory Demyashkin,Matvey Vadyukhin,Zaira M. Murtazalieva,Ekaterina Pugacheva,Vladimir Schekin,Makka B. Bimurzaeva,Svetlana V. Pesegova,Petr Shegay,А. Д. Каприн
出处
期刊:International Journal of Molecular Sciences [MDPI AG]
卷期号:25 (18): 10115-10115
标识
DOI:10.3390/ijms251810115
摘要

Radiotherapy is one of the risk factors for radiation-induced premature ovarian failure and infertility in cancer patients. The development of methods for ovarian radioprotection remains relevant. Moreover, electrons are a little-studied and promising method of radiation with the least toxic effect on normal tissues. The assessment of intracellular mechanisms regulating the protective effects of leukocyte-poor platelet-rich plasma in a model of radiation-induced premature ovarian failure caused by electron irradiation. Wistar rats were divided into four groups, namely a control group, irradiation group (electron exposure), irradiation + leukocyte-poor platelet-rich plasma group, and only leukocyte-poor platelet-rich plasma group. Fragments of ovaries were removed and hormonal, oxidant, histological, and morphometric studies were carried out. The cell cycle of ovarian follicles and the inflammatory and vascular response were assessed using immunohistochemistry. The activity of MAPK, ERK, and PI3K pathways was also assessed using the RT-qPCR. We found that electron irradiation causes a decrease in the functional activity of the ovaries and the death of follicular cells through apoptosis. The administration of LP-PRP led to a partial restoration of the cytokine balance. In addition, minor ovarian damage and mild inflammation were observed in this group. Leukocyte-poor platelet-rich plasma components have anti-inflammatory, angiogenetic, and radioprotective effects, reducing the activation of the NOX4, caspase and cytokine cascades, and inflammatory response severity through the MAPK/p38/JNK signaling pathway. This leads to the induction of endogenous antioxidant protection, the repair of post-radiation follicular damage, and slowing down the development of radiation-induced premature ovarian failure after electron irradiation.
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