CDKN1A down-regulation of inflammasomes and pro-inflammatory cytokines in pyroptosis of cartilage cells

M. Sharma, H. Mishra, S. Singh, K. Longkumer, M. Dhuria
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Abstract

Osteoarthritis is the most common chronic degenerative disease worldwide; it mainly affects elderly people. This disease can involve nearly any joint in the human body, and the most common symptoms include joint pain and disordered articular functions. Inflammasomes (NLRP3) which are induced by nuclear factor kappa B (NF-κB) signaling and can convert interleukin-1β (IL-1β) and IL-18 into mature proinflammatory cytokines are considered a factor in low-grade inflammatory pathology. This study aimed to explore the mechanisms underlying CDKN1A-in osteoarthritis. Chondrocytes were collected and isolated from 22 patients with osteoarthritis (average age 50.22 ± 2.15) and healthy volunteers (average age 51.12 ± 2.34) were enrolled as the control group from June 2021 to June 2023. mRNA expression levels of CDKN1A, NLRP3, and cleaved-Caspase1) were detected by real-time PCR. Cell activity was calculated with CCK-8. It has been found that CDKN1A regulates DNA damage repair, which contributes to the improvement of osteoarthritis by regulating the pyroptosis of cartilage cells. However, the exact mechanistic effects are still unknown.
CDKN1A 下调软骨细胞热解过程中的炎症小体和促炎细胞因子
骨关节炎是全球最常见的慢性退行性疾病,主要影响老年人。这种疾病几乎可累及人体的任何关节,最常见的症状包括关节疼痛和关节功能紊乱。炎症小体(NLRP3)由核因子卡巴B(NF-κB)信号诱导,可将白细胞介素-1β(IL-1β)和IL-18转化为成熟的促炎细胞因子,被认为是低度炎症病理的一个因素。本研究旨在探索 CDKN1A 在骨关节炎中的作用机制。研究采用实时 PCR 技术检测 CDKN1A、NLRP3 和裂解-Caspase1 的 mRNA 表达水平。细胞活性用 CCK-8 计算。研究发现,CDKN1A 可调控 DNA 损伤修复,通过调节软骨细胞的热解作用改善骨关节炎。然而,其确切的机理作用尚不清楚。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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