XXXX cannabinoid receptor agonist inhibits matrix metalloproteinase activity in @entity1566 : A possible mechanism of improved recovery.

@entity66 @entity19 @entity14651 @entity5780 @entity14650 @entity1235 @entity1566
UNASSIGNED: Increased matrix metalloproteinase (MMP) activity contributes to @entity66 formation that inhibits the repair path after @entity1566 ( @entity1566 ). We examined whether treatment with N-   (2-   chloroethyl)-   5Z,   8Z,   11Z,   14Z-   eicosatetraenamide (ACEA), a selective synthetic cannabinoid receptor ( @entity14650 R) agonist, inhibits MMP and improves functional and histological recovery in a @entity19 spinal cord compression injury model. Injured @entity19 randomly received either intraperitoneal ACEA (3mg/kg/day) or vehicle for up to 3 weeks. Behavioral, histological and biochemical assays were performed. Rotarod assessment and the Basso @entity19 Scale score showed an improved performance following ACEA treatment concomitant with a decrease in compression lesion volume. @entity1235 and @entity5780 activity was measured at 1, 7 and 14 days post- @entity1566 . @entity1566 markedly increased @entity1235 , but had negligible effect on @entity5780 activity. ACEA-treatment decreased @entity1235 activity by 80%, 49%, and 56%, respectively (P<0.05) and had a smaller effect on @entity5780 activity. The @entity14650 antagonist SR141716, but not the @entity14651 antagonist SR144528, blocked ACEA-mediated decrease in @entity1235 activity confirming the role of the @entity14650 in the process. Collectively these data demonstrate that post-injury @entity14650 agonism can improve @entity1566 outcome and also indicate marked attenuation of @entity1235 proteolytic enzyme activity as a biochemical mechanism.
