由Nrf2/GPX4调控铁死亡探讨从“瘀”论治激素性骨质疏松症
Treatment of GIOP from stasis theory based on Nrf2/GPX4 regulation of ferroptosis
  
DOI:10.3969/j.issn.1006-7108.2025.01.009
中文关键词:  激素性骨质疏松症  核转录因子-相关因子2  谷胱甘肽过氧化物酶4  铁死亡  瘀证  活血化瘀法  中医中药
英文关键词:glucocorticoid-induced osteoporosis  Nrf2  GPX4  ferroptosis  blood stasis syndrome  blood-activating and stasis-resolving method  traditional Chinese medicine
基金项目:国家自然科学基金项目(82160915);兰州市科技局项目(2022-3-23)
作者单位
樊佳煊1 张维1 崔瑞1 曹林忠1,2* 1.甘肃中医药大学甘肃 兰州 730000 2.甘肃中医药大学附属医院甘肃 兰州 730030 
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中文摘要:
      核转录因子-相关因子2(Nrf2)/谷胱甘肽过氧化物酶4(GPX4)作为胞内关键的抗氧化应激途径,保护多种骨形成相关细胞免受铁死亡的损害,是激素性骨质疏松症(glucocorticoid-induced osteoporosis,GIOP)发病的潜在机制。GIOP因瘀致痹的病机与该系统密切相关,从“瘀”论治的效应可通过该通路轴向调控的微观信息来表达;同时中医治疗GIOP时重视“瘀证”的辨证论治,且临床通常以活血化瘀类、益气活血类中药多见。因此,基于Nrf2/GPX4调控铁死亡探讨从“瘀”论治GIOP的科学性,以“瘀证”为理论指导明确活血化瘀类中药参与Nrf2/GPX4通路调控BMSCs、ECs、OB铁死亡来治疗GIOP,以期为从“瘀”论治GIOP提供科学理论依据,为深入理解GIOP病理生理及临床防治提供新的视角。
英文摘要:
      The nuclear factor-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) pathway, as a crucial intracellular anti-oxidative stress mechanism, prevents various bone formation related cells from ferroptosis damage and represents a potential pathogenic mechanism of glucocorticoid- induced osteoporosis (GIOP). The pathogenesis of GIOP syndrome caused by blood stasis is closely associated with this system. The efficacy of blood stasis treatment can be observed through the microscopic regulation of this pathway. Treatment with traditional Chinese medicine for GIOP emphasizes syndrome differentiation and stasis syndrome treatment, typically utilizing clinical medicine to promote blood circulation, to dissipate blood stasis, and to invigorate qi. Therefore, based on the Nrf2/GPX4 regulation of ferroptosis, this paper discusses the scientific basis for treating GIOP from the perspective of blood stasis, highlighting that traditional Chinese medicine intervention aiming to promote blood circulation and remove blood stasis is involved in regulating ferroptosis in BMSCs, ECs, and OB to treat GIOP. This study offers a novel perspective for comprehending the pathophysiological process of GIOP.
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