Joint Pain and NF-kappaB

NF-kB inhibition found to entirely prevent pain signaling when administered before or during the early stages of knee inflammation

The publication:

October, 2006

The role of spinal nuclear factor-kappa B in spinal hyperexcitability

Summary of the abstract

In behavioral experiments, inhibition of nuclear factor-kappaB activation by systemic administration of the IkappaB kinase inhibitor S1627 has been shown to attenuate inflammatory and neuropathic pain.

Here, we specifically investigated with electrophysiological recordings in anesthetized rats whether spinal application of S1627 influences hyperexcitability of dorsal horn neurons during an acute knee joint inflammation.

Spinal application of S1627 before and early during development of inflammation totally prevented spinal hyperexcitability suggesting an important role of spinal nuclear factor-kappaB in this process.

During established inflammation, however, S1627 did not reduce the responses of neurons to mechanical stimulation of the inflamed knee within 2.5 h after spinal administration, thus suggesting that spinal hyperexcitability is not maintained by continuous nuclear factor-kappaB activation.


Inflammation and pain reduced via NF-kappaB inhibition

When treated with the NF-kB inhibitor early in the course of knee inflammation, or before it begins, the result is “total prevention” of the “hyperexcitability” of the neurons – taken to be an indication of pain signaling.

When inhibition is attempted well into the course of inflammation, no effect is observed. Note that what is being measured is pain. Had the treatment with the NF-kB inhibitor continued for longer than 2.5 hours, inflammation would have been reduced and, with it, response to pain.

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