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Basic Parameter Information

2. Core Mechanism of Action

1. Upregulate the master chondrogenic transcription factor SOX9, boost transcription of core cartilage structural genes including COL2A1 and ACAN, promote continuous synthesis of type II collagen and aggrecan to maintain cartilage elastic structural integrity;
2. Suppress overexpression of matrix catabolic enzymes MMP-13 and ADAMTS-5 triggered by inflammatory stimulation, slow excessive breakdown of extracellular matrix inside damaged joint tissue co-culture models;
3. Stimulate proliferative activity of quiescent chondrocyte precursor cells, raise expression of cell proliferation markers Ki-67 and CD98hc to expand viable cartilage cell populations during long-term incubation cycles;
4. Inhibit apoptosis signaling protein caspase-3, reduce oxidative stress-induced programmed death of chondrocytes and relieve age-related cellular senescence by downregulating senescence markers p16, p21;
5. Balance release of pro-inflammatory mediators in cartilage resident cells, reconstruct a mild non-destructive local microenvironment to cut persistent inflammatory erosion of chondrocyte structures;
6. Optimize metabolic signal communication between chondrocytes and synovial tissue cells, ease abnormal metabolic imbalance induced by simulated mechanical load and chronic inflammatory stress.

3. Core Research Efficacy (For Research Laboratory Use Only)

Chondrocyte Proliferation & Cartilage Matrix Synthesis Research

Degenerative Joint Tissue & Osteoarthritis Cell Model Research

Cartilage Anti-Inflammatory & Lesion Repair Research

Chondrocyte Anti-Senescence & Oxidative Stress Protection Research

Synovial-Chondrocyte Co-Culture Crosstalk Research