Brain ischemia affects
phosphoinositide metabolism and the level of
lipid-derived second messengers.
Phosphatidylinositol transfer proteins (PI-PTs) are responsible for the transport of
phosphatidylinositol (PI) and other
phospholipids through membranes.
Isoform of PI-TPs (PI-TPalpha) is an essential component in ensuring substrate supply for
phospholipase C (PLC). The current study was conducted to examine potential effect of
aniracetam on PI-TPalpha expression and to characterize the PI-TPalpha
isoform distribution between membrane and cytosol fractions of astrocytes exposed to simulated
ischemia in vitro. After 8 h period of
ischemia, the level of PI-TPalpha was significantly higher in cytosol (by about 28%) as well as in membrane fraction (by about 80%) in comparison with control. We have found that
aniracetam treatment of astrocytes in normoxia significantly increased the level of PI-TPalpha in membrane fraction with a maximal effect at 0.1 microM concentration of
aniracetam (by about 195% of control). In membrane fractions of ischemic cells,
aniracetam increased PI-TPalpha expression in a concentration-dependent manner. In ischemic cells,
aniracetam (10 microM) has elevated PI-TPalpha expression up to 155% and 428% in cytosolic and membrane fractions in comparison with ischemic untreated cells, respectively. The study has shown that
aniracetam significantly activates PI-TPalpha in cell membrane fraction and this effect might be connected with previously described activation of MAP kinase cascade.