Glucan Corp. Research Institute, Marine Biotechnology Center, Busan 617-763, Korea.
J Microbiol Biotechnol. 2012 Feb;22(2):274-82. doi: 10.4014/jmb.1110.10078.
The object of this study was to assess the efficacy of Polycan from Aureobasidium pullulans SM-2001, which is composed mostly of beta-1,3-1,6-glucan, on osteoarthritis (OA)-induced by anterior cruciate ligament transection and partial medial meniscectomy (ACLT&PMM). Three different dosages of Polycan (85, 42.5, and 21.25 mg/kg) were orally administered once a day for 84 days to male rats a week after ACLT&PMM surgery. Changes in the circumference and maximum extension angle of each knee, and in cartilage histopathology were assessed using Mankin scores 12 weeks after Polycan administration. In addition, cartilage proliferation was evaluated using bromodeoxyuridine (BrdU). As the result of ACLT&PMM, classic OA was induced with increases in maximum extension angles, edematous knees changes, and capsule thickness, as well as decreases in chondrocyte proliferation, cartilages degenerative changes, and loss of articular cartilage. However, these changes (except for capsule thickness) were markedly inhibited in all Polycan- and diclofenac sodium-treated groups compared with OA control. Although diclofenac sodium did not influence BrdU uptake, BrdU-immunoreactive cells were increased with all dosages of Polycan, which means that Polycan treatment induced proliferation of chondrocytes in the surface articular cartilage of the tibia and femur. The results obtained in this study suggest that 84 days of continuous oral treatment of three different dosages of Polycan led to lesser degrees of articular stiffness and histological cartilage damage compared with OA controls 91 days after OA inducement, suggesting that the optimal Polycan dosage to treat OA is 42.5 mg/kg based on the present study.
本研究旨在评估由出芽被毛孢( Aureobasidium pullulans )SM-2001 产生的聚康( Polycan )的疗效,聚康主要由β-1,3-1,6-葡聚糖组成,用于治疗前交叉韧带切断和部分内侧半月板切除术( ACLT&PMM )引起的骨关节炎( OA )。在 ACLT&PMM 手术后一周,雄性大鼠每天口服一次不同剂量的聚康( 85 、 42.5 和 21.25mg/kg ),持续 84 天。聚康给药 12 周后,通过 Mankin 评分评估每个膝关节的周长和最大伸展角度的变化以及软骨组织病理学变化。此外,使用溴脱氧尿苷( BrdU )评估软骨增殖。由于 ACLT&PMM ,最大伸展角度增加、膝关节肿胀变化和囊厚度增加,以及软骨细胞增殖减少、软骨退行性变化和关节软骨丧失,导致经典 OA 发生。然而,与 OA 对照组相比,所有聚康和双氯芬酸钠治疗组的这些变化(除囊厚度外)均明显受到抑制。虽然双氯芬酸钠对 BrdU 摄取没有影响,但所有剂量的聚康均增加了 BrdU 免疫反应性细胞,这意味着聚康治疗诱导了胫骨和股骨表面关节软骨中软骨细胞的增殖。本研究结果表明,与 OA 诱导后 91 天的 OA 对照组相比,连续口服三种不同剂量的聚康 84 天可导致关节僵硬程度和组织学软骨损伤程度降低,表明根据本研究,治疗 OA 的最佳聚康剂量为 42.5mg/kg 。