通过Fe-curcumin纳米酶介导的反应性氧气物种清理和对与年龄相关的白内障产生抗的作用
Xiang Gao1, Kewei Li1, Yan Huang1
1The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Prevention and Treatment on Major Blinding Diseases, Chongqing Eye Institute, Chongqing Branch (Municipality Division) of the National Clinical Research Center for Ocular Diseases, Chongqing, 400016, PR China.
Materials today. Bio
|June 9, 2025
概括
铁氨酸纳米酶在与年龄相关的白内障 (ARCs) 中表现有前途. 它们减少了氧化应激,细胞衰老和透镜上皮细胞 (LEC) 的炎症,通过准p53通路,有效地延迟了大白在老鼠中的进展.
科学领域:
- 眼科医生 眼科 眼科
- 生物医学工程 生物医学工程
- 细胞生物学 细胞生物学
背景情况:
- 与年龄相关的白内障 (ARCs) 是全球视力障碍的主要原因之一.
- 在透镜上皮细胞 (LEC) 中,氧化应激诱导的衰老和亡是ARC病理的主要驱动因素.
- 目前对ARC的治疗策略有限.
研究的目的:
- 研究Fe-curcumin纳米酶在延缓ARC进展方面的治疗潜力.
- 评估Fe-curcumin纳米酶对LEC细胞衰老,氧化损伤和亡的影响.
- 为了阐明Fe-curcumin纳米酶的潜在分子机制,在ARCs的in vivo大鼠模型中.
主要方法:
- 在新生小鼠中使用了一种酸诱导的氧化应激白内障模型.
- 对H2O处理的LEC进行了体外实验,以评估ROS水平,衰老,亡和抗氧化酶活性 (SOD,CAT).
- 分析了与衰老相关的分泌表型 (SASP) 因子 (IL-6,IL-1β,CXCL1,TGF-β) 和p53/p21/BAX信号轴in vitro和in vivo.
主要成果:
- Fe-curcumin纳米酶显著降低了H2O2处理的LEC中的ROS水平,细胞衰老和细胞亡.
- 纳米酶治疗增加了SOD和CAT水平,并降低了促炎SASP因素的调节.
- 在体内,Fe-curcumin纳米酶通过抑制p53/p21/BAX信号通路,有效地延迟了大鼠的白内障发育.
结论:
- 铁氨酸纳米酶在与年龄相关的白内障中显示出显著的治疗潜力.
- 这些纳米酶通过减轻氧化损伤,细胞衰老和炎症来发挥保护作用.
- 针对与p53相关的途径为开发新型ARC疗法提供了一个有希望的策略.
相关概念视频
Mitochondria
11.4K
Mitochondria are eukaryotic cellular organelles that are known to produce energy through a process called oxidative phosphorylation. Besides their primary function, mitochondria are involved in various cellular processes, including cell growth, differentiation, signaling, metabolism, and senescence. Age-related changes cause a decline in mitochondrial quality and integrity due to increased mitochondrial mutations and oxidative damage. Thus, aging can severely impact mitochondrial functions,...
11.4K
Electron Transport Chain: Complex I and II
12.1K
The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...
ROS generation is regulated and maintained at moderate levels necessary...
12.1K


