Yang Keda, Cao Fangming, Xue Yuchuan, Tao Lin, Zhu Yue
Department of Orthopedics, First Hospital of China Medical University, Shenyang, China.
The First Department of Clinical Medicine, China Medical University, Shenyang, China.
Front Physiol. 2022 Mar 3;13:840293. doi: 10.3389/fphys.2022.840293. eCollection 2022.
Osteoporosis is a common bone imbalance disease that threatens the health of postmenopausal women. Estrogen deficiency accelerates the aging of women. Oxidative stress damage is regarded as the main pathogenesis of postmenopausal osteoporosis. The accumulation of reactive oxygen species in the bone microenvironment plays a role in osteoblast and osteoclast apoptosis. Improving the oxidative state is essential for the prevention and treatment of postmenopausal osteoporosis. There are three classes of antioxidant defense systems in the body to eliminate free radicals and peroxides including antioxidant substances, antioxidant enzymes, and repair enzymes. In our review, we demonstrated the mechanism of antioxidants and their effect on bone metabolism in detail. We concluded that glutathione/oxidized glutathione (GSH/GSSG) conversion involved the PI3K/Akt-Nrf2/HO-1 signaling pathway and that the antioxidant enzyme-mediated mitochondrial apoptosis pathway of osteoblasts was necessary for the development of postmenopausal osteoporosis. Since the current therapeutic effects of targeting bone cells are not significant, improving the systemic peroxidation state and then regulating bone homeostasis will be a new method for the treatment of postmenopausal osteoporosis.
骨质疏松症是一种常见的骨骼失衡疾病，威胁着绝经后女性的健康。雌激素缺乏会加速女性衰老。氧化应激损伤被认为是绝经后骨质疏松症的主要发病机制。骨微环境中活性氧的积累在成骨细胞和破骨细胞凋亡中起作用。改善氧化状态对于绝经后骨质疏松症的预防和治疗至关重要。体内有三类抗氧化防御系统来清除自由基和过氧化物，包括抗氧化物质、抗氧化酶和修复酶。在我们的综述中，我们详细阐述了抗氧化剂的作用机制及其对骨代谢的影响。我们得出结论，谷胱甘肽/氧化型谷胱甘肽（GSH/GSSG）的转化涉及PI3K/Akt-Nrf2/HO-1信号通路，并且抗氧化酶介导的成骨细胞线粒体凋亡途径对于绝经后骨质疏松症的发生发展是必要的。由于目前针对骨细胞的治疗效果不显著，改善全身过氧化状态进而调节骨稳态将成为治疗绝经后骨质疏松症的一种新方法。
