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低分子胶原蛋白肽通过促进软骨细胞细胞外基质合成改善兔前交叉韧带切断模型的骨关节炎进展。

Low-Molecular-Weight Collagen Peptide Ameliorates Osteoarthritis Progression through Promoting Extracellular Matrix Synthesis by Chondrocytes in a Rabbit Anterior Cruciate Ligament Transection Model.

机构信息

Health Food Research and Development, NEWTREE Co., Ltd., Seoul 05604, Republic of Korea.

出版信息

J Microbiol Biotechnol. 2021 Oct 28;31(10):1401-1408. doi: 10.4014/jmb.2108.08027.

Abstract

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 ( < 0.05) improvements of the OARSI score in hematoxylin & eosin (H&E) and Safranin O staining. In microcomputed tomography analysis, LMCP also significantly ( < 0.05) suppressed the deterioration of the microstructure in tibial subchondral bone during OA progression. The elevation of IL-1βand IL-6 concentrations in synovial fluid following OA induction was dose-dependently ( < 0.05) reduced by LMCP treatment. Furthermore, immunohistochemistry illustrated that LMCP significantly ( < 0.05) upregulated type II collagen and downregulated matrix metalloproteinase-13 in cartilage tissue. Consistent with the in vivo results, LMCP significantly ( < 0.05) increased the mRNA expression of and in chondrocytes isolated from a patient with OA regardless of the conditions for IL-1βinduction. These findings suggest that LMCP has potential as a therapeutic treatment for OA that stimulates cartilage regeneration.

摘要

本研究使用兔前交叉韧带切断(ACLT)诱导性 OA 模型和来自 OA 患者的软骨细胞,考察了口服含有 >15%三肽(Gly-X-Y)含量的 3%甘氨酰-脯氨酰-羟脯氨酸(Gly-Pro-Hyp)低分子胶原蛋白肽(LMCP)是否能改善 OA 进展。12 周的口服 LMCP 治疗(100 或 200mg/kg/天)可改善软骨损伤并减少糖胺聚糖的丢失,与 ACLT 对照组相比,OARSI 评分呈剂量依赖性(<0.05)改善,苏木精和伊红(H&E)和番红 O 染色。在 microCT 分析中,LMCP 也显著(<0.05)抑制了 OA 进展过程中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 浓度的升高被 LMCP 治疗呈剂量依赖性(<0.05)降低。此外,免疫组化表明,LMCP 可显著(<0.05)上调软骨组织中 II 型胶原蛋白并下调基质金属蛋白酶-13。与体内结果一致,LMCP 无论在 IL-1β诱导的条件下,均能显著(<0.05)增加来自 OA 患者的软骨细胞中 和 的 mRNA 表达。这些发现表明,LMCP 具有刺激软骨再生的潜力,可能成为 OA 的一种治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d067/9705828/8c9966be2315/jmb-31-10-1401-f1.jpg

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