Markedly, NOV intrathecal treatment abolished CFAinduced MMP-9 expression in both DRG and DHSC, whereas it abrogated MMP-2 induction in DHSC, concomitant with decreased CFA-induced ipsilateral allodynia. The NOV effect was partial but similar to that reported for drugs targeting blockade of NF-B, JNK, IL-1β or TNF-α activities, which partially decrease pain hypersensitivity after CFA injection but fail to induce full recovery from pain symptoms [49,50]. Although the detailed molecular mechanisms involved in the NOV effect remain to be fully understood, these **data** reinforce the hypothesis that NOV exerts an anti-allodynic effect through modulation of MMP-2 and MMP-9. It is noteworthy that NOV treatment is able to reduce allodynia long after CFA administration, when pain symptoms remain robust. This is of clinical interest since studies have yielded debatable results revealing limited efficacies or even ineffectiveness of classical analgesics on mechanical hypersensitivity when administrated in post-CFA treatment [51][52][53][54]. More importantly, the cure of chronic inflammatory pain remains partial [55].