This 2019 study showed that mechanical stress builds up reactive oxygen species in rat cartilage cells, leading to cell death and joint damage. N-acetyl cysteine (NAC), an antioxidant, blocked this in cultured cells, and given by mouth to rats it held back MMP13, the loss of type II collagen and joint damage.
Researchers studied a rat model of joint damage driven by mechanical stress, with a sham-operated comparison side. They measured reactive oxygen species (ROS) and cell death in cartilage cells in the rats, and applied mechanical stress to cultured chondrocytes with and without NAC. They then gave NAC by mouth to the rats and examined joint changes, MMP13, type II collagen and cell death.
Mechanical stress caused ROS to build up in the rats' cartilage cells, leading to cell death and joint damage. In cultured chondrocytes, mechanical stress raised ROS and inflammatory cytokines, and NAC blocked both. NAC by mouth significantly held back joint damage in the rats. It also inhibited MMP13 expression, the fall in type II collagen and chondrocyte cell death. Joint changes on the sham-operated side, which the authors put down to altered weight bearing, were also reduced.
The abstract gives no dose, duration or number of rats, and does not describe the model in detail. Rat joints and lifespans differ from ours. The authors suggest NAC could become an oral option for people, but this study tested only rats.
It links mechanical stress to MMP13 through oxidative stress, and shows an antioxidant taken by mouth interrupting that chain in an animal. MMP13 and type II collagen moved in opposite directions, as they do in several other studies in this library.
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