He Xiao-Feng, Xiong Zhi-Hong, Zhao Qing-Gang, Lei Yi-Hao, Vijayalakshmi Annamalai, Cheng Gang
Pain Department, Affiliated Hospital of Yunnan University (The Second People's Hospital of Yunnan Province, Yunnan Provincial Eye Hospital), Kunming, 650000, China.
Bone and Traumatic Surgery, Affiliated Hospital of Yunnan University (The Second People's Hospital of Yunnan Province, Yunnan Provincial Eye Hospital), Kunming, 650000, China.
Comb Chem High Throughput Screen. 2025;28(8):1363-1371. doi: 10.2174/0113862073286384240227053954.
Osteoarthritis (OA) is a chronic progressive joint ailment that is largely predominant worldwide. However, it typically gets worse over time, occurs more frequently, and becomes more crippling.
Syringic acid (SA) is a well-known phenolic compound reported to suppress inflammation, cell proliferation, and apoptosis of various cancer cells. Since the role of SA in OA remains unknown, there is a need to hypothesize the anti-inflammatory activities of SA on IL- 1β-induced ATDC5 chondrocyte-like cells and to elucidate its protective action against OA.
The cytotoxicity, inflammatory mediators, mRNA expression of MMPs, ADAMTS, COX-2, and Akt/NF-κB protein expression of SA activity on ATDC5 cells were examined through CCK-8 assay, ELISA, RT-qPCR, and western blot. It was found that SA (10, 20, and 30 μM) did not show any inhibitory effects on the viability of the ATDC5 cells in a concentrationdependent manner.
SA markedly reduced the inflammatory mediators, cytokines, PGE2, MMPs, COX-2, and ADAMTS in a concentration-dependent manner. Likewise, SA expressively attenuated IL- 1β-stimulated Akt phosphorylation and NF-κB activation in IL-1β- induced ATDC5 chondrocytes.
This study revealed that SA is a novel candidate applicable for the treatment of OA.
骨关节炎(OA)是一种慢性进行性关节疾病,在全球范围内广泛流行。然而,它通常会随着时间的推移而恶化,发病频率更高,致残性更强。
丁香酸(SA)是一种著名的酚类化合物,据报道可抑制多种癌细胞的炎症、细胞增殖和凋亡。由于SA在OA中的作用尚不清楚,因此有必要推测SA对白细胞介素-1β诱导的ATDC5软骨样细胞的抗炎活性,并阐明其对OA的保护作用。
通过CCK-8法、酶联免疫吸附测定法(ELISA)、逆转录定量聚合酶链反应(RT-qPCR)和蛋白质免疫印迹法检测SA对ATDC5细胞的细胞毒性、炎症介质、基质金属蛋白酶(MMPs)、含血小板反应蛋白基序的解聚素样金属蛋白酶(ADAMTS)的mRNA表达以及Akt/核因子κB(NF-κB)蛋白表达。结果发现,SA(10、20和30μM)对ATDC5细胞的活力没有浓度依赖性的抑制作用。
SA以浓度依赖性方式显著降低炎症介质、细胞因子、前列腺素E2(PGE2)、MMPs、环氧化酶-2(COX-2)和ADAMTS。同样,SA在白细胞介素-1β诱导的ATDC5软骨细胞中显著减弱白细胞介素-1β刺激的Akt磷酸化和NF-κB激活。
本研究表明SA是一种可用于治疗OA的新型候选药物。