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小分子SIRT1激活剂抵消氧化应激诱导的炎症酶激活和在视网膜退化中的核应激

Mengyao Li¹, Qian Xu¹, Qian Fan¹

¹Department of Geriatrics, Qilu Hospital of Shandong University, Jinan, Shandong Province, China; Jinan Clinical Research Center for Geriatric Medicine (202132001), Jinan, Shandong Province, China.

International immunopharmacology

|September 20, 2024

概括

药物学SIRT1激活剂通过抑制NLRP3炎症酶来保护视网膜色素上皮细胞免受氧化损伤. 这些发现表明,与黄斑变性相关的RPE功能障碍的潜在治疗方法.

科学领域:

眼科医生眼科眼科
细胞生物学细胞生物学
药理学药理学是指药理学的学科.

背景情况:

赛尔图因1 (SIRT1) 是一种去乙酶,可以抑制NLRP3炎症酶.
药理学SIRT1激活剂对与年龄相关的黄斑变性 (AMD) 相关的视网膜色素上皮质 (RPE) 细胞损伤的保护作用尚未被探索.

研究的目的:

研究小分子SIRT1激活剂对RPE细胞中氧化和炎症损伤的保护作用.
探索SIRT1激活剂在AMD治疗中的潜在治疗应用.

主要方法:

在体外:ARPE-19细胞用H2O2和SIRT1激活剂 (SRT2104,CAY10602,复星) 进行治疗. 评估细胞死亡,活性氧物种 (ROS),NLRP3炎症组分和炎症性细胞因子 (IL-1β,IL-18). 用SIRT1基因沉默来确认特异性.
在体内:酸盐诱导的视网膜退化小鼠模型被SRT2104或CAY10602.2治疗. 评估了视网膜功能和RPE细胞存活率.

主要成果:

SIRT1激活剂 (SRT2104,CAY10602,复星) 显著降低了H2O2诱导的RPE细胞死亡,ROS积累和核应激.
在受刺激的细胞中,SIRT1激活剂抑制了NLRP3炎症酶激活,包括caspase-1裂变和IL-1β/IL-18产生,这些影响取决于SIRT1.
在体内,治疗改善了视网膜功能,并在视网膜退化的小鼠模型中保存了RPE细胞.

结论:

小分子SIRT1激活剂有效地保护RPE细胞免受氧化应激诱导的NLRP3炎症酶激活.
这些发现凸显了SIRT1激活剂在治疗与黄斑变性相关的RPE功能障碍方面的治疗潜力.

关键词:

与年龄相关的黄斑变性.在NLRP3炎症酶体中,NLRP3炎症氧化应激是一种氧化应激.视网膜色素上皮细胞上皮细胞一个SIRT1系统.一个SIRT1激活器.

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