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姜黄极性提取物对软骨稳态的保护作用:可能的作用机制。

Polar extract of Curcuma longa protects cartilage homeostasis: possible mechanism of action.

机构信息

Department of Biology, R&D Centre, Natural Remedies Private Limited, 5B, Veerasandra Indl. Area, 19th K. M. Stone, Hosur Road, Electronic City Post, Bangalore, Karnataka, 560100, India.

出版信息

Inflammopharmacology. 2018 Oct;26(5):1233-1243. doi: 10.1007/s10787-017-0433-1. Epub 2018 Jan 8.

DOI:10.1007/s10787-017-0433-1
PMID:29313174
Abstract

BACKGROUND

Curcuma longa has been well documented for managing joint inflammation and pain. The present study investigated the effect of polar extract of C. longa (NR-INF-02) on cartilage homeostasis in human articular chondrocytes knee (NHAC-kn) cells to understand its plausible mechanism of action.

METHODS

Dysregulation of cartilage homeostasis was induced by IL-1β and HO. Modulating effects of NR-INF-02 on degradation markers viz., chondrocyte apoptosis, senescence, cytokine, eicosanoids, and cartilage synthesis markers viz., glycosaminoglycans and type II collagen degradation was evaluated in human articular chondrocytes knee (NHAC-kn) cells. Further, the effect of NR-INF-02 on lipopolysaccharide (LPS)-induced expression of NF-kB in RAW264.7 macrophages was investigated.

RESULTS

NR-INF-02 significantly attenuated IL-1β-induced chondrocyte cytotoxicity, apoptosis and release of chondrocyte degradation markers such as IL-6, IL-8, COX-2, PGE, TNF-α, ICAM-1 in NHAC-kn cells. Also, NR-INF-02 protected IL-1β-induced damage to synthesis markers such as glycosaminoglycans, type II collagen and further attenuated HO-induced chondrocyte senescence. In addition NR-INF-02 suppressed LPS-induced NF-kB expression in RAW264.7 cells.

CONCLUSIONS

NR-INF-02 protects cartilage homeostasis by maintaining the balance between synthesis and degradation of cartilage matrix.

摘要

背景

姜黄在管理关节炎症和疼痛方面已有充分的文献记载。本研究调查了长姜极性提取物(NR-INF-02)对人关节软骨细胞(NHAC-kn)软骨内稳态的影响,以了解其可能的作用机制。

方法

通过 IL-1β 和 HO 诱导软骨内稳态失调。在人关节软骨细胞(NHAC-kn)中评估 NR-INF-02 对降解标志物(软骨细胞凋亡、衰老、细胞因子、类花生酸和软骨合成标志物(糖胺聚糖和 II 型胶原降解)的调节作用。此外,还研究了 NR-INF-02 对脂多糖(LPS)诱导 RAW264.7 巨噬细胞中 NF-kB 表达的影响。

结果

NR-INF-02 显著减弱了 IL-1β 诱导的 NHAC-kn 细胞中软骨细胞毒性、凋亡和软骨降解标志物(如 IL-6、IL-8、COX-2、PGE、TNF-α、ICAM-1)的释放。此外,NR-INF-02 保护了 IL-1β 诱导的合成标志物(如糖胺聚糖、II 型胶原)的损伤,并进一步减弱了 HO 诱导的软骨细胞衰老。此外,NR-INF-02 抑制了 LPS 诱导的 RAW264.7 细胞中 NF-kB 的表达。

结论

NR-INF-02 通过维持软骨基质合成和降解之间的平衡来保护软骨内稳态。

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