Blocking NF-kappaB in this model of neuropathic pain eliminated the pain stimulus
The publication:
May, 2009
NF-kappaB mediated enhancement of potassium currents by the chemokine CXCL1/growth related oncogene in small diameter rat sensory neurons
Summary of the abstract or you can read the free full text article
BACKGROUND: Inflammatory processes play important roles in both neuropathic and inflammatory pain states, but the effects of inflammation per se within the sensory ganglia are not well understood.
We examined the direct effects of GRO/KC on small diameter DRG neurons, which are predominantly nociceptive (pain receptors.)
RESULTS: The increase in K currents was completely blocked by co-incubation with protein synthesis inhibitor cycloheximide (CHX) or NF-kappaB inhibitors pyrrolidine dithiocarbamate (PDTC) or quinazoline (6-Amino-4-(4-phenoxypheny lethylamino;QNZ).
CONCLUSION: The results suggest that GRO/KC has important effects in inflammatory processes via its direct actions on sensory neurons, and that activation of NF-kappaB is involved in the GRO/KC-induced enhancement of K currents.
Comments:
Blocking NF-kB prevented the pain fibers from working
This is a technically challenging abstract and much of the jargon has been removed. Nonetheless, it is clear that “GRO/KC” is a key player in the inflammation and pain signals sent by these pain fibers – the “enhanced K currents.”
Activation of NF-kB is “involved” in this GRO/KC effect. So much so, in fact, that by turning off (blocking) NF-kB the effect was eliminated.
Bottom line: in this model, blocking NF-kB blocks pain.
