Chen Ko-Ta, Yeh Chi-Tai, Yadav Vijesh Kumar, Pikatan Narpati Wesa, Fong Iat-Hang, Lee Wei-Hwa, Chiu Yen-Shuo
Department of Orthopedics, Taipei Medical University Hospital, Taipei, 11031, Taiwan.
Department of Medical Research, Shuang Ho Hospital, Taipei Medical University, New Taipei City, 23561, Taiwan.
Heliyon. 2024 Mar 13;10(6):e28094. doi: 10.1016/j.heliyon.2024.e28094. eCollection 2024 Mar 30.
Osteoarthritis (OA), the most prevalent form of arthritis, impacts approximately 10% of men and 18% of women aged above 60 years. Currently, a complete cure for OA remains elusive, making clinical management challenging. The traditional Chinese herb , integral to the Juanbi pill for rheumatism, shows promise in safeguarding chondrocytes through its strong anti-inflammatory effects.
To explore the protective effect of notopterol and miRNA (has-miR-4248) against inflammation, we simulated an inflammatory environment in chondrocytes cell lines C20A4 and C28/12, focusing on inflammasome formation and pyroptosis.
Our finding indicates notopterol significantly reduced interleukin (IL)-18 and tumor necrosis factor (TNF)-alpha levels in inflamed cells, curtailed reactive oxygen species (ROS) production post-inflammation, and inhibited the JAK2/STAT3 signaling pathway, thus offering chondrocytes protection from inflammation. Importantly, notopterol also hindered inflammasome assembly and pyroptosis by blocking the NF-κB/NLRP3 pathway through hsa-miR-4282 modulation. experiments showed that notopterol treatment markedly decreased Osteoarthritis Research Society International (OARSI) scores in OA mice and boosted hsa-miR-4282 expression compared to control groups.
This study underscores notopterol's potential as a therapeutic agent in OA treatment, highlighting its capacity to shield cartilage from inflammation-induced damage, particularly by preventing pyroptosis.
骨关节炎(OA)是最常见的关节炎形式,影响着约10%的60岁以上男性和18%的60岁以上女性。目前,OA的完全治愈仍然难以实现,这使得临床管理具有挑战性。传统中药,是治疗风湿的蠲痹丸的主要成分,因其强大的抗炎作用,在保护软骨细胞方面显示出前景。
为了探究羌活醇和微小RNA(hsa-miR-4248)的抗炎保护作用,我们在软骨细胞系C20A4和C28/12中模拟炎症环境,重点关注炎性小体的形成和细胞焦亡。
我们的研究结果表明,羌活醇显著降低了炎症细胞中白细胞介素(IL)-18和肿瘤坏死因子(TNF)-α的水平,减少了炎症后活性氧(ROS)的产生,并抑制了JAK2/STAT3信号通路,从而为软骨细胞提供抗炎保护。重要的是,羌活醇还通过调节hsa-miR-4282阻断NF-κB/NLRP3途径,阻碍炎性小体的组装和细胞焦亡。实验表明,与对照组相比,羌活醇治疗显著降低了OA小鼠的国际骨关节炎研究学会(OARSI)评分,并提高了hsa-miR-4282的表达。
本研究强调了羌活醇在OA治疗中作为治疗药物的潜力,突出了其保护软骨免受炎症诱导损伤的能力,特别是通过防止细胞焦亡。