found transient PDE2A mRNA upregulation after hind paw inflammation that was accompanied by enhanced acute mechanical paw withdrawal latencies, which indicated that PDE2A likely contributed to acute radicular inflammation and pain .
Furthermore, we gained insights into whether PDE2A is involved in the underlying mechanisms of the treatment of pain by low-concentration [O.sub.3] therapy.
PDE2A and NF-[kappa]B/p65 mRNA were measured by RT-PCR.
The protein expressions of PDE2A and NF-[kappa]B/p65 were analyzed by western blotting.
20[micro]g/mL [O.sub.3] Downregulated the Overexpression of Spinal PDE2A and NF-[kappa]B/p65 in Chronic Radiculitis Rats.
There is general consensus that PDE2A is abundant in the central nervous system of mammals, especially in the laminae I and II of spinal dorsal horn in rats [20, 34].
Furthermore, 20 [micro]g/mL [O.sub.3] decreases the overexpression of PDE2A and NF-[kappa]B/p65 while also upregulates cGMP and cAMP.