Department of Orthopedics, South of Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Huangcun, Daxing District, Beijing 100053, China.
Department of Emergency, People's Hospital of Beijing Daxing District, Daxing District, Beijing 102600, China.
Acta Biochim Pol. 2022 Feb 7;69(1):65-69. doi: 10.18388/abp.2020_5634.
In the present study isoxanthanol was investigated for treatment of monosodium iodoacetate (MIA)-induced osteoarthritis (OA) in vivo. The study demonstrated that isoxanthanol inhibited excessive release of interleukin-6, NO and PGE2 in RAW264.7 cells treated with LPS in dose dependent manner. The effects of isoxanthanol were examined in a rat model of osteoarthritis (OA) and observed to amelio-rate inflammatory damage and protect against OA. Moreover, in vivo data also confirmed inhibition of interleukin-6, NO and PGE2 levels in LPS-induced OA-rats. Deterioration of knee subchondral bone in LPS-induced OA-rats was also prevented effectively by isoxanthanol-treatment. Therefore, isoxanthanol prevents subchondral bone deterioration in OA rats via targeting inflammatory processes.
本研究考察了异山梨醇对体内单碘乙酸盐(MIA)诱导的骨关节炎(OA)的治疗作用。研究表明,异山梨醇可抑制 LPS 诱导的 RAW264.7 细胞中白细胞介素-6、NO 和 PGE2 的过度释放,并呈剂量依赖性。在骨关节炎(OA)大鼠模型中观察到异山梨醇的作用,可减轻炎症损伤并预防 OA。此外,体内数据还证实了异山梨醇对 LPS 诱导的 OA 大鼠中白细胞介素-6、NO 和 PGE2 水平的抑制作用。异山梨醇治疗还可有效防止 LPS 诱导的 OA 大鼠膝关节软骨下骨的恶化。因此,异山梨醇通过靶向炎症过程预防 OA 大鼠的软骨下骨恶化。