Department of Pharmacology and Clinical Pharmacology, Medical Faculty, Uludağ University, 16059, Bursa, Turkey.
Neurochem Res. 2010 Mar;35(3):429-36. doi: 10.1007/s11064-009-0075-9. Epub 2009 Oct 13.
Incubation of rat cortical slices in a medium that was not containing oxygen and glucose (oxygen-glucose deprivation, OGD) caused a 200% increase in the release of S100B. However, when slices were transferred to a medium containing oxygen and glucose (reoxygenation conditions, or REO), S100B release reached 500% of its control value. Neither inhibition of nitric oxide (NO) synthase by L-NAME nor addition of the NO donors sodium nitroprussid (SNP) or hydroxylamine (HA) to the medium altered basal S100B release. Similarly, the presence of SNP, HA or NO precursor L: -arginine in the medium, or inhibition of NO synthase by L-NAME also failed to alter OGD- and REO-induced S100B outputs. Moreover, individual inhibition of PKC, PLA(2) or PLC all failed to attenuate the S100B release determined under control condition or enhanced by either OGD or REO. Blockade of calcium channels with verapamil, chelating the Ca(+2) ions with BAPTA or blockade of sodium channels with tetrodotoxin (TTX) did not alter OGD- and REO-induced S100B release. In contrast to the pharmacologic manipulations mentioned above, glutamate and alpha-ketoglutarate added at high concentrations to the medium prevented both OGD- and REO-induced S100B outputs. These results indicate that neither NO nor the activation of PKC, PLA(2) or PLC seem to be involved in basal or OGD- and REO-induced S100B outputs. Additionally, calcium and sodium currents that are sensitive to verapamil and TTX, respectively, are unlikely to contribute to the enhanced S100B release observed under these conditions.
在不含氧和葡萄糖的培养基中孵育大鼠皮质切片（氧葡萄糖剥夺，OGD）会导致 S100B 的释放增加 200%。然而，当切片转移到含有氧和葡萄糖的培养基中（再氧合条件，或 REO）时，S100B 的释放达到对照值的 500%。NO 合酶的抑制剂 L-NAME 的抑制作用，以及向培养基中添加 NO 供体硝普钠（SNP）或羟胺（HA），均未改变基础 S100B 的释放。同样，NO 前体 L：精氨酸在培养基中的存在，或 L-NAME 对 NO 合酶的抑制作用，也未能改变 OGD 和 REO 诱导的 S100B 产物。此外，单独抑制蛋白激酶 C（PKC）、磷脂酶 A2（PLA2）或磷脂酶 C（PLC）均未能减弱在对照条件下确定的或由 OGD 或 REO 增强的 S100B 释放。用维拉帕米阻断钙通道、用 BAPTA 螯合 Ca（+2）离子或用河豚毒素（TTX）阻断钠通道，均未改变 OGD 和 REO 诱导的 S100B 释放。与上述药理学操作相反，在培养基中添加高浓度的谷氨酸和α-酮戊二酸可防止 OGD 和 REO 诱导的 S100B 产物的释放。这些结果表明，NO 以及 PKC、PLA2 或 PLC 的激活似乎都不参与基础或 OGD 和 REO 诱导的 S100B 产物的释放。此外，分别对维拉帕米和 TTX 敏感的钙电流和钠电流不太可能对这些条件下观察到的 S100B 释放增加做出贡献。
