Roth Andreas, Mollenhauer Jürgen, Wagner Andreas, Fuhrmann Reneè, Straub Albrecht, Venbrocks Rudolf A, Petrow Peter, Bräuer Rolf, Schubert Harald, Ozegowski Jörg, Peschel Gundela, Müller Peter J, Kinne Raimund W
Department of Orthopaedics, Rudolf-Elle Hospital, Friedrich Schiller University Jena, Eisenberg, Germany.
Arthritis Res Ther. 2005;7(3):R677-86. doi: 10.1186/ar1725. Epub 2005 Mar 31.
To assess the potential use of hyaluronic acid (HA) as adjuvant therapy in rheumatoid arthritis, the anti-inflammatory and chondroprotective effects of HA were analysed in experimental rat antigen-induced arthritis (AIA). Lewis rats with AIA were subjected to short-term (days 1 and 8, n = 10) or long-term (days 1, 8, 15 and 22, n = 10) intra-articular treatment with microbially manufactured, high-molecular-weight HA (molecular weight, 1.7 x 10(6) Da; 0.5 mg/dose). In both tests, 10 buffer-treated AIA rats served as arthritic controls and six healthy animals served as normal controls. Arthritis was monitored by weekly assessment of joint swelling and histological evaluation in the short-term test (day 8) and in the long-term test (day 29). Safranin O staining was employed to detect proteoglycan loss from the epiphyseal growth plate and the articular cartilage of the arthritic knee joint. Serum levels of IL-6, tumour necrosis factor alpha and glycosaminoglycans were measured by ELISA/kit systems (days 8 and 29). HA treatment did not significantly influence AIA in the short-term test (days 1 and 8) but did suppress early chronic AIA (day 15, P < 0.05); however, HA treatment tended to aggravate chronic AIA in the long-term test (day 29). HA completely prevented proteoglycan loss from the epiphyseal growth plate and articular cartilage on day 8, but induced proteoglycan loss from the epiphyseal growth plate on day 29. Similarly, HA inhibited the histological signs of acute inflammation and cartilage damage in the short-term test, but augmented acute and chronic inflammation as well as cartilage damage in the long-term test. Serum levels of IL-6, tumour necrosis factor alpha, and glycosaminoglycans were not influenced by HA. Local therapeutic effects of HA in AIA are clearly biphasic, with inhibition of inflammation and cartilage damage in the early chronic phase but with promotion of joint swelling, inflammation and cartilage damage in the late chronic phase.
为评估透明质酸（HA）作为类风湿性关节炎辅助治疗的潜在用途，在实验性大鼠抗原诱导性关节炎（AIA）中分析了HA的抗炎和软骨保护作用。将患有AIA的Lewis大鼠进行短期（第1天和第8天，n = 10）或长期（第1天、第8天、第15天和第22天，n = 10）关节内注射微生物制造的高分子量HA（分子量，1.7×10⁶Da；0.5mg/剂量）治疗。在两项试验中，10只接受缓冲液治疗的AIA大鼠作为关节炎对照，6只健康动物作为正常对照。在短期试验（第8天）和长期试验（第29天）中，通过每周评估关节肿胀和组织学评估来监测关节炎。采用番红O染色检测关节炎膝关节骨骺生长板和关节软骨中蛋白聚糖的丢失。通过ELISA/试剂盒系统测量血清白细胞介素-6、肿瘤坏死因子α和糖胺聚糖水平（第8天和第29天）。HA治疗在短期试验（第1天和第8天）中对AIA没有显著影响，但确实抑制了早期慢性AIA（第15天，P<0.05）；然而，在长期试验（第29天）中，HA治疗倾向于加重慢性AIA。HA在第8天完全防止了骨骺生长板和关节软骨中蛋白聚糖的丢失，但在第29天诱导了骨骺生长板中蛋白聚糖的丢失。同样，HA在短期试验中抑制了急性炎症和软骨损伤的组织学迹象，但在长期试验中增加了急性和慢性炎症以及软骨损伤。血清白细胞介素-6、肿瘤坏死因子α和糖胺聚糖水平不受HA影响。HA在AIA中的局部治疗效果明显呈双相性，在早期慢性阶段抑制炎症和软骨损伤，但在晚期慢性阶段促进关节肿胀、炎症和软骨损伤。
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