实验大鼠卵巢血管缺血再灌注后的卵巢功能障碍

K. Nariai, R. Fukumoto, Shin Onota, Ken Watanabe, H. Uchiyama, K. Kanayama, Kahei Sato
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摘要

活性氧(ROS)的过量产生导致组织或器官的氧化应激功能障碍。为了证实ROS对卵巢功能障碍的影响,本研究采用实验大鼠对卵巢血管进行缺血再灌注(I/R)处理。研究了超氧化物歧化酶(SOD)作为自由基清除剂对卵巢I/R损伤的预防作用。卵巢对马绒毛膜促性腺激素(eCG)和人绒毛膜促性腺激素(hCG)的激素敏感性在I/R后下降。卵巢组织和卵子也被破坏。这些变化可以通过SOD来预防。我们的数据表明,与ROS产生相关的I/R损伤导致卵巢功能障碍。这种功能障碍可以通过使用根治性清除剂来预防。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Ovarian dysfunction after ischemia-reperfusion of the ovarian blood vessel in experimental rats
Excessive production of reactive oxygen species (ROS) lead to oxidative stress in tissue or organ dysfunction. To confirm ovarian dysfunction by ROS, ischemia-reperfusion (I/R) treatment of the ovarian blood vessels was performed using experimental rats in this study. Preventive effect of superoxide dismutase (SOD) as a radical scavenger against ovarian I/R injury was also examined. Hormonal sensitivities to equine chorionic gonadotropin (eCG) and human chorionic gonadotropin (hCG) in the ovary decreased after the I/R. Ovarian tissue and ovum destruction were also observed. These changes could be prevented by SOD administration. Our data suggest that I/R injury related to ROS production causes ovarian dysfunction. The dysfunction is prevented by administration of a radical scavenger.
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