Cytochalasin D (CD) is known as a disruptor of actin cytoskeleton architecture in chondrocytes. We have studied the role of CD in retinoic acid (RA) caused dedifferentiation and inflammation responses in rabbit articular chondrocytes. We have examined the effect of CD on RA induced dedifferentiation of chondrocytes. CD inhibited RA induced dedifferentiation determined by Western blot analysis and Alcian blue staining in rabbit articular chondrocytes. Also, CD additionally reduced inflammation response molecules such as cyclooxygenase-2 (COX-2) and prostaglandin $E_2$ ($PGE_2$) in RA treated cells. Treatment of CD reduced phosphorylation of p38 by treatment of RA. Inhibiton of p38kinase with SB203580 reduced expression of COX-2 and production of $PGE_2$ by treatment of CD in RA treated cells. But, Inhibiton of p38kinase with SB203580 did not any relationship with effect of CD on RA caused dedifferentiation. In summary, our results indicate that CD regulates RA reduced expression of COX-2 and production of PGE2 via p38kinase pathway.