This 2017 lab study exposed rat cartilage cells to the inflammatory signal IL-1 beta, with or without curcumin. Curcumin blocked the activation of NF-kB, a switch for inflammatory genes. That went with lower MMP13 and higher type II collagen, and cells given curcumin grew more than cells given IL-1 beta alone.
The researchers grew articular chondrocytes from rats and treated them with interleukin-1 beta, with or without curcumin or a known NF-kB blocker, pyrrolidine dithiocarbamate. They measured type II collagen, MMP13 and the NF-kB pathway proteins IκBα, its phosphorylated form and p65/RelA, as protein and as RNA, tracked whether p65 moved into the nucleus, and measured cell growth with a CCK-8 assay.
Curcumin stopped IL-1 beta from switching on NF-kB, by blocking the phosphorylation of IκBα and the move of p65/RelA into the nucleus. That went with lower MMP13 expression and higher type II collagen expression, both of which NF-kB controls. Cells treated with curcumin alongside IL-1 beta grew more than cells given IL-1 beta alone.
These are rat cells in a dish, and the abstract does not give the curcumin concentration or the length of treatment. Curcumin went straight onto the cells, so the study does not show whether enough reaches cartilage when a person eats it. Rat cartilage cells can respond differently from human ones.
It traces a clear route from an inflammatory signal to MMP13, and shows curcumin interrupting it at NF-kB. The collagen the enzyme targets went up rather than down, so the experiment captures both sides: less of the cutting enzyme and more of the collagen it cuts.
In lab and animal studies, yes. Curcumin lowered MMP13 in rat cartilage cells exposed to IL-1 beta, and a curcumin metabolite bound and blocked MMP13 directly and...
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...