Hyaluronic acid is a long sugar molecule found in joint fluid and cartilage. In human cartilage cells it lowered IL-1 beta-driven MMP13, more at higher doses.
Also called hyaluronan, HA, sodium hyaluronate.
The key MMP13 study is from 2011. Julovi and colleagues took cartilage cells from people with osteoarthritis or rheumatoid arthritis and stimulated them with IL-1 beta, which raised MMP13 through the p38 signalling route (Julovi 2011).
Adding hyaluronan lowered both MMP13 and activated p38, in a dose-dependent way across 0.1 to 4 mg/ml. At 4 mg/ml it cut p38 activation by more than 60% (Julovi 2011). Blocking CD44, hyaluronan's principal receptor, significantly reversed the effect, which showed the route it works through (Julovi 2011).
This is a cell study. It shows how hyaluronan can act on cartilage cells in a dish at those concentrations, not what an oral dose does in a joint. No other study on this site tests hyaluronan against MMP13.
Yes, in lab studies. The inflammatory messenger IL-1 raised MMP13 in human cartilage and cartilage cells in several studies, and TNF-alpha did too. To switch the MMP13...
In two main ways. Cells release MMP13 as an inactive proenzyme that must be cut before it works, and the body makes its own inhibitors, the TIMPs. TIMP-1, TIMP-2 and...