Non-Steroidal anti-inflammatory
drugs ease the acute inflammatory reaction and impair pro inflammatory events
dependent on neutrophils but their main action is to inhibit cyclo-oxyganase,
which are accountable for prostaglandin biosynthesis. There are two kind of COX,
COX1 is theoretically dependable for homeostatic function of PGs and COX2 are
important in PGE, production during inflammation.
This study focused
on two NSAIDs drug named meloxicam (MXC) and diclofenac (DCF). The experiment
was done on rabbit with antigen-induced arthritis that they were treated with
MXC, DCF and control group. The results showed that, these two drug reduced
arthritis due to down regulated interleukin 8(IL8) production but they did not
prevent the monocyte chemotactic peptide-1 (MCP-1). Both IL8 and MCP-1 over
expression in the rheumatoid synovial tissue cause the arthritis progression.
These chemokines correlated with the severity of leucocyte infiltration.
Both drugs
reduced PGE levels and the polymorphonuclear cells (PMN)
Concentration in
synovial fluid, in other hand mononuclear cells (MN) concentration was not
change at all in treated group but their data showed there was increased in MNN
density due to active expression of MCP-1 in synovial membrane.
This study showed
that, depletion a total PGE might not be pleasing because NASIDs reduced IL8 in
arthritis but it also help MN recruitment, so there should be more research on
this field.
Side note: PMN and MN are both white blood cells. MN
cells contain lymphocytes, monocytes and macrophages and PMN cell contain
neutrophils, basophils and esoinophils.
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