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(Synonyms: 溴米那; Bromovalerylurea) 目录号 : GC33694

Bromisoval (Bromovalerylurea, Isobromyl, Bromaral, BRN 1773255) is a hypnotic and sedative of the bromoureide group with anti-inflammatory effects.

Bromisoval (Bromovalerylurea) Chemical Structure

Cas No.:496-67-3

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10mM (in 1mL DMSO)
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1g
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实验参考方法

Kinase experiment:

Conditioning media are obtained from BV2 cell cultures that have been incubated for 24 h in E2 medium containing 1 μg/ml LPS, with or without Bromisoval (BU) (1-100 μg/mL) or other agents, and subjected to NO determination. To normalize the releasing NO level by the cellular protein contents, cells are solubilized with RIPA buffer (50 mM Tris-HCl, pH 8.0, 150 mM sodium chloride, 0.5% w/v sodium deoxycholate, 0.1% w/v sodium dodecyl sulfate, 1.0% w/v NP-40 substitute) and the protein contents are determined by BCA protein assay reagents[1].

Cell experiment:

Murine microglial cell line BV2 is used. BV2 cells are maintained in medium supplemented with 10% fetal bovine serum. BV2 cells are seeded onto wells in 4-well culture plates and incubated with LPS for 30 min to 24 h. When the effects of Bromisoval (BU) or other agents are investigated, BV2 cells are incubated with the appropriate agent (e.g. Bromisoval) for 30 min before the addition of LPS[1].

Animal experiment:

Suspensions of the compounds (including Bromisoval ) in aqueous 0.5% carboxymethyl cellulose are administered intraperitoneally to adult male albino mice weighing 25-35 g. All tests are performed on groups of ten mice[2].

References:

[1]. Kawasaki S, et al. Effects of hypnotic bromovalerylurea on microglial BV2 cells. J Pharmacol Sci. 2017 Jun;134(2):116-123.
[2]. Mrongovius RI, et al. Comparison of the bromureide sedative-hypnotic drugs, bromvaletone (bromisoval) and carbromal, and their chloro analogues in mice. Clin Exp Pharmacol Physiol. 1976 Sep-Oct;3(5):443-7.

产品描述

Bromisoval (Bromovalerylurea, Isobromyl, Bromaral, BRN 1773255) is a hypnotic and sedative of the bromoureide group with anti-inflammatory effects.

Chemical Properties

Cas No. 496-67-3 SDF
别名 溴米那; Bromovalerylurea
Canonical SMILES CC(C)C(Br)C(NC(N)=O)=O
分子式 C6H11BrN2O2 分子量 223.07
溶解度 DMSO : 300 mg/mL (1344.87 mM) 储存条件 Store at -20°C
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Research Update

Effects of hypnotic Bromovalerylurea on microglial BV2 cells

J Pharmacol Sci 2017 Jun;134(2):116-123.PMID:28645489DOI:10.1016/j.jphs.2017.05.007.

An old sedative and hypnotic Bromovalerylurea (BU) has anti-inflammatory effects. BU suppressed nitric oxide (NO) release and proinflammatory cytokine expression by lipopolysaccharide (LPS)-treated BV2 cells, a murine microglial cell line. However, BU did not inhibit LPS-induced nuclear translocation of nuclear factor-κB and subsequent transcription. BU suppressed LPS-induced phosphorylation of signal transducer and activator of transcription 1 (STAT1) and expression of interferon regulatory factor 1 (IRF1). The Janus kinase 1 (JAK1) inhibitor filgotinib suppressed the NO release much more weakly than that of BU, although filgotinib almost completely prevented LPS-induced STAT1 phosphorylation. Knockdown of JAK1, STAT1, or IRF1 did not affect the suppressive effects of BU on LPS-induced NO release by BV2 cells. A combination of BU and filgotinib synergistically suppressed the NO release. The mitochondrial complex I inhibitor rotenone, which did not prevent STAT1 phosphorylation or IRF1 expression, suppressed proinflammatory mediator expression less significantly than BU. BU and rotenone reduced intracellular ATP (iATP) levels to a similar extent. A combination of rotenone and filgotinib suppressed NO release by LPS-treated BV2 cells as strongly as BU. These results suggest that anti-inflammatory actions of BU may be attributable to the synergism of inhibition of JAK1/STAT1-dependent pathways and reduction in iATP level.

Bromovalerylurea modulates GABAA receptor-mediated inhibitory neurotransmission while inducing sleep

Biochem Biophys Res Commun 2023 Jan 1;638:176-183.PMID:36462491DOI:10.1016/j.bbrc.2022.11.062.

Bromovalerylurea (BU), an acyl urea derivative, was originally developed as a hypnotic/sedative. We recently reported that BU at a dose of 50 mg/kg ameliorates sepsis, Parkinson's disease, and traumatic brain injury in Wistar rat models through its anti-inflammatory actions on microglia and macrophages. However, since BU was developed more than 100 years ago, its hypnotic mechanism and characteristics are poorly understood. Herein, we conducted an electroencephalogram (EEG) study and found that BU, when administered at a dose of more than 125 mg/kg but not at a dose of 50 mg/kg in Wistar rats, significantly increased non-rapid eye movement (NREM) sleep duration and dose-dependently decreased rapid eye movement (REM) sleep duration. This characteristic of sleep induced by BU is similar to the effect of compounds such as barbiturate, benzodiazepine, and z-drugs, all of which require γ-aminobutyric acid A receptors (GABAAR) for hypnotic/sedative activity. To investigate whether BU could potentiate GABAAergic neurotransmission, we conducted a whole-cell patch-clamp recording from pyramidal neurons in rat cortical slices to detect spontaneous GABAAR-mediated inhibitory postsynaptic currents (IPSCs). We found that BU dose-dependently prolonged IPSCs. Importantly, the prolonged IPSCs were not attenuated by flumazenil, a benzodiazepine receptor antagonist, suggesting that modulation of IPSCs by BU is mediated by different mechanisms from that of benzodiazepine. Taken together, these data elucidate the basic characteristics of the hypnotic effects of BU and suggest that the enhancement of GABAAR-mediated Cl- flux may be a possible mechanism that contributes to its hypnotic/sedative activity.

Myoclonic jerks due to acute Bromovalerylurea intoxication

Clin Toxicol (Phila) 2008 Nov;46(9):861-3.PMID:18668386DOI:10.1080/15563650802020361.

Background: Bromides are still sold as sedatives, antitussives, and anticonvulsants in many countries. Bromovalerylurea is a bromide-containing sedative-hypnotic that is occasionally combined with non-steroidal anti-inflammatory drugs in over-the-counter products. Chronic intake of excessive Bromovalerylurea can produce bromide intoxication, but acute Bromovalerylurea intoxication presenting with myoclonic jerks has never been described. Case report: A 23-year-old woman was brought to our emergency department with unusual drowsiness. Her physical examination was normal except for frequent myoclonic jerks in all extremities that could be triggered by moving the patient or by noxious stimuli. Initial blood tests results were normal; the serum bromide concentration was 81.0 mg/L (reference <10 mg/L). Treatment with intravenous normal saline and furosemide resulted in gradual improvement in her drowsiness and myoclonic jerks. By the second hospital day, she was normal. A brain magnetic resonance imaging (MRI) was normal. At a 2-month follow-up visit, the patient had no neurological sequelae. Discussion: Chronic bromide intoxication caused by long-term abuse of Bromovalerylurea may present as psychiatric or neurologic abnormalities. Our case of acute Bromovalerylurea intoxication presented with severe myoclonic jerks and lethargy. The serum bromide concentration was similar to the reported concentrations in acute bromide intoxications. Treatment with normal saline and diuretics results in increased clearance of bromide and an improvement in clinical effects. Conclusion: Myoclonic jerks may be one of the major presentations of acute Bromovalerylurea intoxication. Physicians should consider bromide intoxication in the differential diagnosis of the causes of myoclonic jerks.

The hypnotic Bromovalerylurea ameliorates 6-hydroxydopamine-induced dopaminergic neuron loss while suppressing expression of interferon regulatory factors by microglia

Neurochem Int 2016 Oct;99:158-168.PMID:27392596DOI:10.1016/j.neuint.2016.06.013.

The low molecular weight organic compound Bromovalerylurea (BU) has long been used as a hypnotic/sedative. In the present study, we found that BU suppressed mRNA expression of proinflammatory factors and nitric oxide release in lipopolysaccharide (LPS)-treated rat primary microglial cell cultures. BU prevented neuronal degeneration in LPS-treated neuron-microglia cocultures. The anti-inflammatory effects of BU were as strong as those of a synthetic glucocorticoid, dexamethasone. A rat hemi-Parkinsonian model was prepared by injecting 6-hydroxydopamine into the right striatum. BU was orally administered to these rats for 7 days, which ameliorated the degeneration of dopaminergic neurons in the substantia nigra pars compacta (SNpc) and alleviated motor deficits. BU suppressed the expression of mRNAs for interferon regulatory factors (IRFs) 1, 7 and 8 in the right (lesioned) ventral midbrain as well as those for proinflammatory mediators. BU increased mRNA expression of various neuroprotective factors, including platelet-derived growth factor and hepatocyte growth factor, but it did not increase expression of alternative activation (M2) markers. In microglial culture, BU suppressed the LPS-induced increase in expression of IRFs 1 and 8, and it reduced LPS-induced phosphorylation of JAK1 and STATs 1 and 3. Knockdown of IRFs 1 and 8 suppressed LPS-induced NO release by microglial cells. These results suggest that suppression of microglial IRF expression by BU prevents neuronal cell death in the injured brain region, where microglial activation occurs. Because many Parkinsonian patients suffer from sleep disorders, BU administration before sleep may effectively ameliorate neurological symptoms and alleviate sleep dysfunction.

Comparison of the detrimental features of microglia and infiltrated macrophages in traumatic brain injury: A study using a hypnotic Bromovalerylurea

Glia 2018 Oct;66(10):2158-2173.PMID:30194744DOI:10.1002/glia.23469.

Microglia and blood-borne macrophages in injured or diseased brains are difficult to distinguish because they share many common characteristics. However, the identification of microglia-specific markers and the use of flow cytometry have recently made it easy to discriminate these types of cells. In this study, we analyzed the features of blood-borne macrophages, and activated and resting microglia in a rat traumatic brain injury (TBI) model. Oxidative injury was indicated in macrophages and neurons in TBI lesions by the presence of 8-hydroxy-2'-deoxyguanosine (8-OHdG). Generation of mitochondrial reactive oxygen species (ROS) was markedly observed in granulocytes and macrophages, but not in activated or resting microglia. Dihydroethidium staining supported microglia not being the major source of ROS in TBI lesions. Furthermore, macrophages expressed NADPH oxidase 2, interleukin-1β (IL-1β), and CD68 at higher levels than microglia. In contrast, microglia expressed transforming growth factor β1 (TGFβ1), interleukin-6 (IL-6), and tumor necrosis factor α at higher levels than macrophages. A hypnotic, Bromovalerylurea (BU), which has anti-inflammatory effects, reduced both glycolysis and mitochondrial oxygen consumption. BU administration inhibited chemokine CCL2 expression, accumulation of monocytes/macrophages, 8-OHdG generation, mitochondrial ROS generation, and proinflammatory cytokine expression, and markedly ameliorated the outcome of the TBI model. Yet, BU did not inhibit microglial activation or expression of TGFβ1 and insulin-like growth factor 1 (IGF-1). These results indicate that macrophages are the major aggravating cell type in TBI lesions, in particular during the acute phase. Activated microglia may even play favorable roles. Reduction of cellular energy metabolism in macrophages and suppression of CCL2 expression in injured tissue may lead to amelioration of TBI.