| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | HEK 293 cells |
Preparation Method | Preceding the addition of drugs, cultures were washed once with warm phosphate-buffered saline and then exposed to various treatments in Dulbecco s modified Eagle s medium supplemented with sodium pyruvate (1 mM). Cultures were then exposed to control medium, vehicle, or varying concentrations of FCCP (5 µM, 500 nM, or 50 nM in 0.05% ethanol) or baf A1 (1 µM in dimethyl sulfoxide). Four hours after addition of drugs, the medium was removed. |
Reaction Conditions | FCCP (5 µM, 500 nM, or 50 nM in 0.05% ethanol) for 4 hours |
Applications | FCCP inhibits APP catabolism but not maturation |
| 产品描述 | FCCP, a proton carrier (H+ ionophore), is also a powerful phosphoric acid defusing coupling agent, which promotes the depolarization of plasma membrane and mitochondrial membrane.FCCP can affect various activities in which cellular calcium ions participate, inhibit K+ background current and induce small inward current, decrease 0.1 unit pH, and induce intracellular Na+ to increase. FCCP can stimulate Mg2+-ATPase activity, inhibit β-amyloid formation, and simulate the physiological effect of glutamate receptor agonist NMDA on mitochondrial superoxide. Exposure of K695sw cells to the protonophore FCCP resulted in a concentration-dependent decrease in both Aβ release and the formation of the cell-associated C99 fragment. Production of the ectodomain fragment APPsα was only affected by exposure to the highest concentration of FCCP, whereas neither total cellular levels of APP nor the maturation of APP via N /O -linked glycosylation appeared to be affected by any concentration of FCCP used[1]. Pre-exposure to 200 nM FCCP during 120 min protects and enhances the follicle integrity in cat ovarian tissue during short-term in vitro culture[2]. Concentrations of FCCP that cause mitochondrial oxidation without depolarisation are cardioprotective. Higher FCCP concentrations dissipate mitochondrial membrane potential and exacerbate injury[3]. FCCP activated ionic currents and depolarized the plasma membrane potential in a dose-dependent manner. Neither the removal of extracellular Ca2+ nor pretreatment with BAPTA/AM affected the FCCP-induced currents, implying that the currents are not associated with the FCCP-induced intracellular [Ca2+]i increase[4]. Application of FCCP evoked a gradual increase in cell body [Ca2+]i that reached a level approximately 3-fold higher than baseline after 60 min. Moreover, FCCP released Ca2+ even when added after mitochondrial stores of Ca2+ had previously been emptied by an alternate method. FCCP, in addition to its recognized effect on mitochondrial Ca2+ sequestration, also releases Ca2+ from a non-mitochondrial store and is, therefore, unsuitable for use in an intact neuron to selectively inactivate mitochondrial Ca2+ uptake[5]. A further analysis of this effect on BHK21 cells has shown that a decrease in the number of microtubules can be observed 15 min after adding FCCP and there is complete disruption after 60 min. Regrowth of microtubules was initiated 30 min after removal of FCCP, in marked contrast with the rapid reversion observed when microtubules are disrupted by nocodazole[6]. References: |
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