Role of ATP-sensitive potassium channels and inflammatory response of basilar artery smooth muscle cells in subarachnoid hemorrhage of rabbit and immune-modulation by shikonin.

To investigate the role of inflammatory response, oxidative damage and changes of ATP-sensitive potassium channels (sK_ATP) in basilar artery (BA) smooth muscle cells (SMCS) of rabbits in subarachnoid hemorrhage (SAH) model.

Time course studies on inflammatory response by real-time PCR, oxidative process and function of isolated basilar artery after SAH in New Zealand White rabbits were performed. Basilar artery smooth muscle cells (BASMCs) in each group were obtained and whole-cell patch-clamp technique was applied to record cell membrane capacitance and K_ATP currents. The morphologies of basal arteries were analyzed. Protective effect of shikonin were also determine by same parameters.

Inflammatory cytokines levels were highest at 24h compare to 72h after SAH whereas the oxidative damage and cell death marker were at highest peak at 72h. Oxidative damage peak coincided with significant alterations in cell membrane capacitance, K_ATP currents and morphological changes in basilar arteries. Shikokin pretreatment attenuated early inflammatory response at 24h and associated oxidative damage at 72h. Finally, shikonin attenuated morphological changes in basilar arteries and dysfunction.

Currents of ATP-sensitive potassium channels in basilar smooth muscle cells decreased after SAH by putative oxidative modification from immediate inflammatory response and can be protected by shikonin pretreatment.