| 包装: | 1mg |
| 市场价: | 1124元 |
Cell lines | NK cell |
Preparation Method | Cells were then treated with either 1 μM Ionomycin free acid or DMSO, as vehicle control, and cultured for 16 hours. Control and ionomycin-treated cells were then washed and allowed to rest for 24 hours at 2x106 cells/mL in RPMI 10% FBS. |
Reaction Conditions | 1 μM Ionomycin free acid for 16 hours |
Applications | Human NK cells treated with Ionomycin free acid lose their ability to degranulate and secrete IFN-γ in response to a variety of stimuli, but IL-2 stimulation can compensate these defects. |
Animal models | Athymic nude mice (Balb/c nu/nu female, 6 to 8 weeks old) |
Preparation Method | The effects of intratumoral injection of Ionomycin free acid on the growth of subcutaneous HT1376 tumors established in athymic nude mice were then tested. |
Dosage form | Intratumoral injection 100 ug Ionomycin free acid 3 times a week for 4 weeks |
Applications | Intratumoral injection of Ionomycin free acid into subcutaneous HT1376 tumors reduced the tumorigenicity in nude mice. |
| 产品描述 | Ionomycin free acid is a selective and potent calcium ion carrier that acts as an active Ca2+ carrier. By stimulating the entry of storage-regulated cations across biofilms, effectively improves Ca2+ influx[9]. Human NK cells treated with Ionomycin free acid lose their ability to degranulate and secrete IFN-γ in response to a variety of stimuli, but IL-2 stimulation can compensate these defects[2]. When tested hypothesis by hyperpolarizing HL-60 cells using Ionomycin free acid before electroporation. Hyperpolarizing cells before electroporation alters the pulsed electric field intensity thresholds for reversible electroporation and IRE, allowing for greater control and selectivity of electroporation outcomes[3]. Ionomycin free acid induces calcium influx into the intracellular region and reactive oxygen species production in N1E-115 cells. Lipid hydroperoxide production was induced in ionomycin-treated N1E-115 cells[5]. Ionomycin free acid, at least in part, exerts its effects via specific binding to a G-protein coupled receptor, thereby evoking downstream cellular events like arachidonate release with subsequent prostaglandin formation[6]. A high concentration of Ionomycin free acid increased the frequency and amplitude of calcium oscillation patterns, affecting the balance of mitochondrial energy metabolism, leading to increased reactive oxygen species (ROS) and decreased ATP[1]. Intratumoral injection of Ionomycin free acid into subcutaneous HT1376 tumors reduced the tumorigenicity in nude mice. Furthermore, these in vivo growth-inhibitory effects of Ionomycin free acid were significantly enhanced by pretreatment with cisplatin[8]. Acetylcholine (ACh) evoked secretion by the calcium ionophore, ionomycin, was studied at frog motor nerve endings. Bath application of Ionomycin free acid stimulated an irreversible increase in the rate of spontaneous, quantal ACh release in the presence of extracellular Ca2+. In contrast, local application of Ionomycin free acid stimulated a rapid, reversible acceleration of spontaneous ACh release[4]. Following stimulation with Ionomycin free acid, PD-1+ICOS+ CD4+ T cells expressed significantly lower IL-17A, but not IFNγ, levels in GF BXD2 mice compared to SPF BXD2 mice[7]. References: |
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