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GYY4137诱导的p65硫化通过改善骨质关节炎发展中的线粒体功能来保护突巨细胞免受热

Jun Ma¹, Peng Yang², Zhibin Zhou³

¹Department of Orthepaedics, Naval Medical Center of PLA, Naval Medical University, Shanghai, China; Department of Health Statistics, Naval Medical University, Shanghai, China; Department of Orthopaedic Trauma Surgery, Shanghai Changzheng Hospital, Naval Medical University, Shanghai, China.

Journal of advanced research

|June 6, 2024

概括

GYY4137,一种硫化 (H2S) 捐赠体,通过抑制巨细胞中 pyroptosis 和 NLRP3 炎症酶激活来缓解骨关节炎 (OA). 它通过修改NF-kB p65蛋白来实现这一目标,提供了潜在的新型OA治疗方法.

科学领域:

生物化学生物化学
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

骨关节炎 (OA) 涉及渐进的突炎症和软骨损失.
硫化 (H2S) 供体GYY4137在OA中显示出抗炎作用的潜力,但其机制尚不清楚.

研究的目的:

为了验证GYY4137对OA的保护作用.
阐明GYY4137在OA的行动背后的监管机制.

主要方法:

在体外研究中使用了小鼠原发性冠状细胞和RAW 264.7巨细胞.
在体内研究中使用了DMM诱导的OA小鼠模型和巨细胞特定的p65淘汰小鼠.
技术包括细胞传染,免疫光,EDU检测,电子显微镜和分子检测 (qPCR,西部斑).

主要成果:

在体内,GYY4137通过抑制协同膜质炎症来减轻OA.
在体外,GYY4137降低了炎症诱导的NLRP3和caspase-1激活,降低了IL-1β的产生.
GYY4137增加了NF-kB p65的硫化,减少了ROS和改善了线粒体功能;H2S在p65中硫化氨酸38,抑制了其活性.

结论:

GYY4137通过p65的氧化还原修饰抑制OA诱导的NLRP3激活,调节炎症反应.
GYY4137为骨关节炎治疗提供了一个有前途的治疗策略.

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