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.
*NR-INF-02 ( Turmacin)
Salient features of the study:
1.The main feature of osteoarthritis (OA) is damage to the tissue known as articular cartilage.
2. Ageing, trauma, mechanical stress, metabolic syndrome causes rupture of cartilage homeostasis via promoting synthesis of cartilage damaging factors.
3. Turmacin (NR-INF-02) has been investigated for its effects on restoring cartilage homeostasis via inhibiting cartilage damaging factors.
4. Turmacin (NR-INF-02) inhibited cartilage damaging pathways/factors such as NF-kB, IL-1beta, IL-6, IL-8, TNF-alfa, ICAM-1, COX-2 and PGF2 and protected glycosaminoglycans and collagen, which are the structural components of cartilage.
Methods
Dysregulation of cartilage homeostasis was induced by IL-1β and H2O2. 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, PGE2, 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 H2O2-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.
Publication: Inflammopharmacology Experimental and Therapeutic Studies ( Springer )To view full text , please refer : http://rdcu.be/ElZ8
