School of Pharmacy, Sungkyunkwan University, Gyeonggi-do 440-746, Korea.
Biol Pharm Bull. 2010;33(6):1004-10. doi: 10.1248/bpb.33.1004.
This study investigated the effect of human placenta extract (HPE) on cartilage degradation in vitro MG-63 cells, articular cartilage explants, and in vivo monoiodoacetate (MIA)-induced osteoarthritis (OA). Matrix metalloproteinase (MMP)-2 activity was measured in HPE-treated osteoblastic MG-63 cells. Articular cartilage explants in rabbit were cultured, and the degree of proteoglycan (PG) degradation was assessed by measuring the amount of glycosaminoglycan (GAG) released into the culture medium. Experimental osteoarthritis was induced by intra-articular injection of 3 mg MIA in rats. Beginning 14 d post-MIA injection, HPE was administered intra-articularly once a day for 14 d. The knee joints were assessed by roentgenography, histology, and gelatinase activity. HPE inhibited PG degradation in articular cartilage explants. HPE significantly reduced deformity of knee joints and suppressed the histological change in MIA-induced OA. HPE inhibited MMP-2 activity in MG-63 cells. MMP-2 and -9 activities were also reduced in the cartilages of HPE-treated knee joints. Our results indicate that HPE has therapeutic effects on OA by protecting cartilage.
本研究探讨了人胎盘提取物（HPE）对体外 MG-63 细胞、关节软骨标本和体内单碘乙酸（MIA）诱导的骨关节炎（OA）中软骨降解的影响。测定 HPE 处理的成骨细胞 MG-63 细胞中基质金属蛋白酶（MMP）-2 的活性。培养兔关节软骨标本，通过测量释放到培养基中的糖胺聚糖（GAG）量来评估蛋白聚糖（PG）降解程度。通过向大鼠关节内注射 3 mg MIA 诱导实验性 OA。自 MIA 注射后 14 天开始，每天一次关节内给予 HPE 治疗 14 天。通过 X 线摄影、组织学和明胶酶活性评估膝关节。HPE 抑制关节软骨标本中 PG 的降解。HPE 显著减轻了膝关节畸形，并抑制了 MIA 诱导的 OA 的组织学变化。HPE 抑制了 MG-63 细胞中的 MMP-2 活性。HPE 处理的膝关节软骨中 MMP-2 和 -9 的活性也降低。我们的结果表明，HPE 通过保护软骨对 OA 具有治疗作用。
