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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.

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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