Department of Sports Medicine and Rehabilitation, Shandong First Medical University (Shandong Academy of Medical Sciences), Taian, Shandong, China.
The Second Affiliated Hospital of Shandong First Medical University, Taian, Shandong, China.
Cell Signal. 2024 Jan;113:110960. doi: 10.1016/j.cellsig.2023.110960. Epub 2023 Nov 15.
Osteoarthritis (OA) is a degenerative joint disease commonly found in middle-aged and older people. Chondrocytes are the only cells in joint cartilage that are difficult to heal after pyroptosis, and they will aggravate the wear and tear of joint cartilage and affect the progression of OA. Pyroptosis is a novel form of programmed cell death, and the classical pyroptosis pathway is a programmed cell death pattern mediated by inflammatory cysteine protease-1. Activation of NLRP3 leads to activation and cleavage of caspase-1 precursors, which in turn leads to activation and cleavage of GSDMD proteins and the release of proinflammatory factors. Resolvin D1 (RvD1) is a specialized pro-resolving mediator (SPM) derived from omega-3 unsaturated fatty acids that reduces inflammation and catabolic responses in OA chondrocytes. However, it is unclear whether RvD1 promotes OA chondrocyte proliferation and thus joint cartilage repair. Our results show that RvD1 regulates the NLRP3/caspase-1 signaling pathway by inhibiting the expression of caspase-1, promoting the proliferation of OA chondrocytes, promoting the repair of articular cartilage in rats and delaying the progression of osteoarthritis.
骨关节炎（OA）是一种常见于中老年人的退行性关节疾病。软骨细胞是关节软骨中唯一难以在细胞焦亡后修复的细胞，它们会加重关节软骨的磨损，影响 OA 的进展。细胞焦亡是一种新型的程序性细胞死亡形式，经典的细胞焦亡途径是一种由炎性半胱天冬酶-1 介导的程序性细胞死亡模式。NLRP3 的激活导致 caspase-1 前体的激活和切割，进而导致 GSDMD 蛋白的激活和切割以及促炎因子的释放。消退素 D1（RvD1）是一种源自ω-3 不饱和脂肪酸的特异性促解决介质（SPM），可减轻 OA 软骨细胞中的炎症和分解代谢反应。然而，尚不清楚 RvD1 是否促进 OA 软骨细胞增殖，从而促进关节软骨修复。我们的结果表明，RvD1 通过抑制 caspase-1 的表达来调节 NLRP3/caspase-1 信号通路，促进 OA 软骨细胞的增殖，促进大鼠关节软骨的修复，并延缓骨关节炎的进展。
