酸路径调节由化物诱导的软细胞的氧化损伤和亡
Fang-Fang Yu1, Huan-Xia Zhang1, Kang-Ting Luo2
1Department of Environmental Health, School of Public Health, Zhengzhou University, 100 Kexue Avenue, Zhengzhou, Henan 450001, China.
Ecotoxicology and environmental safety
|January 28, 2026
概括
化物暴露会通过抑制酸路径 (PPP) 触发胆细胞亡和氧化损伤. 用AG1激活PPP显著减轻了这些对软骨的有害影响.
科学领域:
- 生物化学 生物化学
- 细胞生物学 细胞生物学
- 毒理学 毒理学 毒理学
背景情况:
- 化症是一种系统性疾病,影响骨和牙健康,通常涉及软骨病变.
- 冠状细胞亡和氧化损伤是骨化的关键病理特征.
研究的目的:
- 调查酸通路 (PPP) 在化物诱导的状细胞亡和氧化损伤中的作用.
- 探索激活PPP对软骨中化物毒性的治疗潜力.
主要方法:
- 对基因表达综合数据集 (GSE70719) 的生物信息学分析,以确定化物诱导的骨细胞损伤中的丰富途径.
- 在体外研究中,使用暴露于化 (NaF) 的细胞和老鼠关节软骨.
- 评估PPP活性,尼古丁胺胺氨基二核酸盐 (NADPH) 和谷氨 (GSH) 水平以及亡标志物.
- 用AG1,一种葡萄糖-6-酸盐脱酶激动剂进行治疗,以评估其保护作用.
主要成果:
- 生物信息学分析显示,在化物诱导的骨细胞损伤中,PPP的丰富程度显著.
- 化 (NaF) 抑制了冠状细胞PPP活性,降低了NADPH和GSH水平,并增强了亡和氧化损伤.
- 暴露于NaF也抑制了PPP,并促进了大鼠关节软骨的亡.
- AG1治疗显著增加了PPP活性,并减轻了NaF诱导的慢性细胞亡和氧化损伤.
结论:
- NaF抑制PPP,导致NADPH和GSH水平降低,氧化应激增加,随后导致冠状细胞亡和氧化损伤.
- 用AG1激活PPP提供了一种潜在的治疗策略,以减轻化物诱导的软骨损伤.
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