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目的探究钾依赖钠/钙交换蛋白-6(SLC24A6)参与大鼠脑出血后继发性脑损伤的作用和可能机制。方法建立SD大鼠脑出血模型,检测大鼠脑出血后尾状核SLC24A6表达及其介导的细胞内钙浓度([Ca~(2+)]_i)随时间变化的情况,观察SLC24A6在正常氧浓度和低氧条件下对[Ca~(2+)]_i的调控。结果脑出血早期,尾状核SLC24A6蛋白和SLC24A6mRNA水平均降低,在脑出血后3 d降至最低水平,5和7 d后轻微升高。脑出血后早期,[Ca~(2+)]_i增加,于脑出血后3 d达最高水平,5和7 d时逐步下降。正常氧浓度下,转染SLC24A6导致HEK293[Ca~(2+)]_i升高。结论 SLC24A6通过抑制钙超载在脑出血后脑损伤中起保护作用。
Objective To investigate the role of potassium-dependent sodium / calcium exchanger-6 (SLC24A6) in secondary brain injury following intracerebral hemorrhage in rats and its possible mechanism. Methods The model of intracerebral hemorrhage in SD rats was established. The expression of SLC24A6 in the caudate nucleus and the change of intracellular Ca2 + concentration ([Ca2 +] i) in the rat caudate nucleus after ICH were measured. Regulation of [Ca ~ (2 +)] _i under oxygen and hypoxic conditions. Results The level of SLC24A6 protein and SLC24A6 mRNA in caudate nucleus decreased at the early stage of cerebral hemorrhage. The levels of SLC24A6 protein and SLC24A6 mRNA decreased to the lowest level 3 d after cerebral hemorrhage and slightly increased at 5 and 7 d. Early after cerebral hemorrhage, [Ca ~ (2 +)] _ i increased, reaching the highest level on the 3rd day after intracerebral hemorrhage and gradually decreased on the 5th and 7th day. Transfection with SLC24A6 resulted in elevation of HEK293 [Ca ~ (2 +)] _i at normal oxygen concentration. Conclusion SLC24A6 plays a protective role in the brain injury after intracerebral hemorrhage by inhibiting calcium overload.