【摘要】 目的　在人胚肾细胞 (HEK2 93cells)研究容积性钙内流和花生四烯酸激活性钙内流的相互作用。方法　采用荧光探针Fura2 /AM技术测定HEK2 93细胞内钙对花生四烯酸、Thapsigargin反应变化。结果　容积性钙内流可被花生四烯酸明显抑制 ,花生四烯酸所致钙内流亦可被容积性钙内流激动剂所抑制 ,这种交互抑制并非由药物化学性互相影响 ,肌浆网钙泵的抑制 ,钙池耗竭 ,或来自于容积性钙内流本身。相反 ,这种抑制可能与容积性钙内流激活过程和花生四烯酸激活过程相互作用有关。结论　容积性钙内流与花生四烯酸所致的钙内流呈现相互抑制作用 ,这种抑制可防止细胞出现中毒性钙超载更多还原

【Abstract】 Objective To examine the interaction between capacitative calcium entry and arachidonic acid activated calcium entry, which co exist in non excitable cells.Methods In human embryonic kidney cells (HEK293 cells), the intracellular Ca 2+ concentration ([Ca 2+ ] i) in response to thapsigargin and arachidonic acid were measured by using acetoxymethyl ester of Fura 2 (Fura 2/AM).Results Both thapsigargin and arachidonic acid produced Ca 2+ release from the same intracellular Ca 2+ stores and Ca 2+ entry from extracellular space. These two Ca 2+ entry pathways exhibited mutual antagonism. The inhibition did not appear to result from a direct action of thapsigargin, from inhibition of SERCA pumps or depletion of Ca 2+ stores, or from entry of Ca 2+ through capacitative calcium entry channels.Conclusion It appeared that a discrete step in the pathway signaling capacitative calcium entry interacted with and inhibited the arachidonic acid pathway. The occurrence of mutual antagonism between the two distinct calcium entry pathways may provide protection for the cell against toxic Ca 2+ overload.更多还原