BAPTA-AM is a well-known membrane permeable Ca(2+) chelator. The externally applied BAPTA-AM inhibited hERG channels in a concentration-dependent manner (IC(50): 1.3 microM). BAPTA-AM inhibited hKv1.3 and hKv1.5 channels in a concentration-dependent manner (IC(50): 1.45 and 1.23 microM, respectively), and the blockade of these two types of channels was also dependent on channel opening[3]. BAPTA-AM (BAPTA/AM), an intracellular calcium chelator, induces delayed necrosis by lipoxygenase-mediated free radicals in mouse cortical cultures. Mixed cortical cell cultures (DIV 13-16) exposed to 10 μM BAPTA-AM for 24- or 48-hr show moderate (45-70%) neuronal injury as evaluated by increased LDH release into the bathing medium after 24-48-hr. Exposure of cortical cultures to 3-10 μM BAPTA-AM for 48-hr evoke dose-dependent neuronal damage[4]. BAPTA-AM inhibit osteoclastogenic ability of BMMs via suppressing the increase of [Ca(2+)](i) which lead to inhibit RANKL-induced the phosphorylation of ERK, Akt and p38 MAPK, but not JNK[5]. BAPTA-AM can decrease cellular pH and inhibit acidocalcisome acidification in starved cells[6].
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