The role of prostaglandins in experimental arthritis in the rat

Abstract

In the experimental model of streptococcal CFE-induced arthritis, PGE and PGF concentrations rise significantly. This is due to an increase both in the substrate concentration and the enzyme activity for PG biosynthesis. Indomethacin therapy inhibited PG synthesis and diminished some of the gross, but not the histological, features of the inflammatory response. These results lend further support to the contention that the beneficial effect of indomethacin in arthritis is due to inhibition of PG biosynthesis.