| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | BV - 2 cell lines |
Preparation Method | SCH 23390 hydrochloride was added to B-2 cell medium. |
Reaction Conditions | 1uM SCH 23390 hydrochloride hydrochloride |
Applications | As DRD1 and DRD2 inhibitor, SCH 23390 hydrochloride hydrochloride is able to reverse the isosibiricin-mediated inhibition of the NLRP3/caspase-1 inflammasome pathway. |
Animal models | Adult female CD-1 mice |
Preparation Method | To examine the potential mechanisms by which high-dose DA induces ductus constriction, isolated vessels were first exposed to newborn oxygen conditions before receiving pretreatment with 10-6M of a DA1-like receptor antagonist (SCH 23390 hydrochloride), followed by exposure to increasing concentrations of DA. |
Dosage form | Pretreat isolated ductus with 10-6 M SCH 23390 hydrochloride |
Applications | SCH 23390 hydrochloride augments dopamine-induced ductus constriction in CD-1 mouse vessels under newborn O2 conditions. |
| 产品描述 | SCH 23390 hydrochloride is a highly potent and selective dopamine D1-like receptor antagonist with a K(i) of 0.2 and 0.3 nM for the D1 and D5 dopamine receptor subtypes, respectively. In vitro, it also binds with high affinity to the 5-HT2 and 5-HT1C serotonin receptor subtypes[1].As a potent and high efficacy human 5-HT2C receptor agonist with a Ki of 9.3 nM. SCH-23390 hydrochloride inhibits G protein-coupled inwardly rectifying potassium (GIRK) channels with an IC50 of 268 nM[2,3]. SCH 23390 hydrochloride (1 μM) treatment reverses the inhibitory effects of Isosibiricin on NLRP3 expression and the cleavages of caspase-1 and IL-1β in the LPS-induced BV-2 cells. SCH 23390 hydrochloride could reverse the Isosibiricin-mediated inhibition of the NLRP3/caspase-1 inflammasome pathway[4].Pretreatment of primary astrocytes with the DRD1 antagonistSCH 23390 hydrochloride did not reduce cabergoline induced GSH synthesis[6]. In spontaneously hypertensive rats, fenoldopam produced a dose-dependent reduction in arterial pressure and a significant increase in mesenteric and renal blood flow, and pretreatment with the DA 1-like receptor antagonist SCH 23390 hydrochloride significantly attenuated these effects[5]. C57BL/6J mice were injected with the D1R antagonist SCH 23390 hydrochloride, and a decrease in social behavior was seen, producing autism-like behavior[7]. The effects of Aβ on memory in Per2 mice were investigated, and the increased Aβ levels did not influence the memory performance of Per2 mice after SCH 23390 hydrochloride treatment[9].SCH 23390 hydrochloride and Haloperidolwere administered during CPP. The accompanying changes in phosphorylation of extracellular signal-regulated kinase (ERK) in MLDS related brain regions, including the ventral tegmental area (VTA), caudate putamen (CPu), prefrontal cortex (PFC), and nucleus accumbens (NAc) were measured in the CPP mice. Results revealed that 60% N2O induced CPP in the gas-administered mice and promoted the ERK phosphorylation (p-ERK) in the NAc and CPu during the test session of the CPP test. Pretreatment of SCH 23390 hydrochloride(0.5 mg/kg) inhibited the acquisition of N2O-induced CPP and the enhanced p-ERK in NAc[8]. References: |
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