Shenzhen Pingle Orthopedic Hospital (Shenzhen Pingshan Traditional Chinese Medicine Hospital), 40 Jintang Street, Luohu District, Shenzhen, 518010, Guangdong Province, People's Republic of China.
J Orthop Surg Res. 2020 Apr 16;15(1):150. doi: 10.1186/s13018-020-01648-z.
To evaluate the repairing effects of glucosamine sulfate combined with etoricoxib on articular cartilages of patients with knee osteoarthritis (KOA).
A total of 106 KOA patients were randomly divided into control (n = 40) and experimental groups (n = 66) and treated with etoricoxib alone and glucosamine sulfate plus etoricoxib, respectively. Changes in WOMAC score and clinical efficacy were observed. The synovial fluid was extracted. Bone metabolism indices, growth factors, inflammatory factors, matrix metalloproteinases (MMPs), and NO-induced apoptosis-related factors were measured by ELISA. JNK and Wnt5a mRNA levels were determined using RT-PCR.
After treatment, the total WOMAC scores of both groups significantly declined (P < 0.05), being lower in experimental group. The total effective rate of experimental group was higher (P < 0.05). BGP and OPG levels rose, especially in experimental group (P < 0.05). CTX-II, COMP, and RANKL levels decreased, particularly in experimental group (P < 0.05). TGF-β, IGF-1, and FGF-2 levels increased, especially in experimental group (P < 0.05). Both groups, particularly experimental group, had decreased levels of IL-1β, IL-17, IL-18, TNF-α, MMP-3, MMP-9, and MMP-13 (P < 0.05). JNK and Wnt5a mRNA levels of both groups dropped, which were lower in experimental group (P < 0.05). NO and LPO levels reduced, being lower in experimental group. SOD level rose, especially in experimental group (P < 0.05).
Glucosamine sulfate plus etoricoxib can repair the articular cartilages of KOA patients. Probably, JNK and Wnt5a are downregulated to inhibit the secretion of MMPs through lowering the levels of inflammatory factors, thereby delaying cartilage matrix degradation. NO-induced chondrocyte apoptosis may be suppressed via the SOD pathway.
评估硫酸氨基葡萄糖联合依托考昔对膝骨关节炎（KOA）患者关节软骨的修复作用。
将 106 例 KOA 患者随机分为对照组（n = 40）和实验组（n = 66），分别给予依托考昔单药和硫酸氨基葡萄糖联合依托考昔治疗，观察 WOMAC 评分和临床疗效的变化。抽取关节滑液，采用 ELISA 法测定骨代谢指标、生长因子、炎症因子、基质金属蛋白酶（MMPs）、NO 诱导的凋亡相关因子，采用 RT-PCR 法测定 JNK 和 Wnt5a mRNA 水平。
治疗后两组的 WOMAC 总分均显著下降（P < 0.05），实验组更低。实验组的总有效率更高（P < 0.05）。BGP 和 OPG 水平升高，实验组更明显（P < 0.05）。CTX-II、COMP 和 RANKL 水平降低，实验组更明显（P < 0.05）。TGF-β、IGF-1 和 FGF-2 水平升高，实验组更明显（P < 0.05）。两组，尤其是实验组，IL-1β、IL-17、IL-18、TNF-α、MMP-3、MMP-9 和 MMP-13 水平均降低（P < 0.05）。两组 JNK 和 Wnt5a mRNA 水平下降，实验组更低（P < 0.05）。NO 和 LPO 水平降低，实验组更低。SOD 水平升高，实验组更明显（P < 0.05）。
硫酸氨基葡萄糖联合依托考昔可修复 KOA 患者的关节软骨。可能是通过降低炎症因子水平下调 JNK 和 Wnt5a，抑制 MMPs 的分泌，从而延缓软骨基质降解。NO 诱导的软骨细胞凋亡可能通过 SOD 途径被抑制。
