This study examined whether the oral administration of low-molecular-weight collagen peptide (LMCP) containing 3% Gly-Pro-Hyp with >15% tripeptide (Gly-X-Y) content could ameliorate osteoarthritis (OA) progression using a rabbit anterior cruciate ligament transection (ACLT) model of induced OA and chondrocytes isolated from a patient with OA. Oral LMCP administration (100 or 200 mg/kg/day) for 12 weeks ameliorated cartilage damage and reduced the loss of proteoglycan compared to the findings in the ACLT control group, resulting in dose-dependent (P < 0.05) improvements of the OARSI score in hematoxylin & eosin and Safranin O staining. In micro-computed tomography analysis, LMCP also significantly (P < 0.05) suppressed the deterioration of the microstructure in tibial subchondral bone during OA progression. The elevation of IL-1β and IL-6 concentrations in synovial fluid following OA induction were dose-dependently (P < 0.05) reduced by LMCP treatment. Furthermore, immunohistochemistry illustrated that LMCP significantly (P < 0.05) upregulated type II collagen and downregulated matrix metalloproteinase-13 in cartilage tissue. Consistent with the in vivo results, LMCP significantly (P < 0.05) increased the mRNA expression of COL2A1 and ACAN in chondrocytes isolated from a patient with OA regardless of the conditions for IL-1β induction. These findings suggest that LMCP has potential as a therapeutic treatment for OA that stimulates cartilage regeneration.

中文翻译：

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低分子量胶原蛋白肽通过在兔前交叉韧带横断模型中促进软骨细胞合成细胞外基质来改善骨关节炎进展。

本研究使用兔前交叉韧带检查口服含 3% Gly-Pro-Hyp 和 >15% 三肽 (Gly-XY) 含量的低分子量胶原肽 (LMCP) 是否可以改善骨关节炎 (OA) 进展诱导的 OA 和从 OA 患者分离的软骨细胞的横切 (ACLT) 模型。与 ACLT 对照组相比，口服 LMCP（100 或 200 mg/kg/天）12 周后软骨损伤得到改善并减少了蛋白多糖的损失，导致 OARSI 评分呈剂量依赖性（P < 0.05）改善在苏木精和伊红以及番红 O 染色中。在显微计算机断层扫描分析中，LMCP 也显着 ( P< 0.05) 在 OA 进展过程中抑制了胫骨软骨下骨微观结构的恶化。OA 诱导后滑液中 IL-1β 和 IL-6 浓度的升高通过 LMCP 治疗呈剂量依赖性 ( P < 0.05) 降低。此外，免疫组织化学表明 LMCP 显着 ( P < 0.05) 上调软骨组织中的 II 型胶原蛋白和下调基质金属蛋白酶 13。与体内结果一致，LMCP 显着（P < 0.05）增加了COL2A1和ACAN的 mRNA 表达在从 OA 患者分离的软骨细胞中，无论 IL-1β 诱导的条件如何。这些发现表明 LMCP 具有作为刺激软骨再生的 OA 治疗方法的潜力。