Rosiglitazone is currently used in the treatment of type 2 diabetes and is suggested to be a perspective medicine for neurodegenerative diseases as a regulator of inflammation in central nervous system. The present work is focused on rosiglitazone effect on inflammatory response stimulated by lipopolysaccharide (LPS) in rat astroglioma cells line C6 and primary rat astrocytes. We have estimated the effect at the cyclooxygenase 2 (COX-2) mRNA expression level by qPCR and at the level of signal molecules prostaglandin E?2 (PGE2) release by ELISA method. LPS has been shown to induce the expression of COX-2 mRNA and the PGE?2 release in both glioma cells and primary astrocytes correlating with data previously obtained. The effects of rosiglitazone have been proved out to be opposite. In glioma cells rosiglitazone prevents the COX-2 expression induction and decreases the level of PGE2 release. On the contrary, rosiglitazone increases the inflammatory response stimulated by LPS in primary astrocytes showing pro-inflammatory properties rather than anti-inflammatory. Rosiglitazone alone does not affect the COX-2 expression in glioma but increase PGE2 synthesis activity, while this substance induces the inflammatory response in primary astrocytes. Our data suggest the large differences between mechanisms of rosiglitazone action in inflammatory response in glioma and primary cells opening a new look at drug signaling research in cancer cells.