| 包装 | 价格(元) |
| 1mg | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
Cell lines | Neuronal cells |
Preparation Method | Studies were initiated in cultures at days 10 to 12 in vitro by exchanging the culture medium with a low-magnesium balanced salt solution.10 Peptides and drugs were added from concentrated stocks 15 minutes before the addition of NMDA. |
Reaction Conditions | Treated neuronal cell cultures with 100 μmol/L NMDA for 30 minutes together with Tat-NR2B9c over a range of concentrations: 0, 0.05, 0.1, 0.5 μmol/L. |
Applications | Tat-NR2B9c showed neuroprotectant efficacy in patients with acute stroke. Tat-NR2B9c is designed to uncouple NO production from NMDAr activation by blocking PSD-95 binding to NMDAr and nNOS. Tat-NR2B9c also prevents NMDA-induced superoxide p47phox formation by blocking phosphorylation. |
Animal models | Timed pregnant CD1 mice (7-day-old (P7) pups of either sex) |
Preparation Method | Tat-NR2B9c was administered intraperitoneally at a single dose of 15 μg/g body weight in 100–120 μl of saline. |
Dosage form | 15 μg/g |
Applications | Tat-NR2B9c has a neuroprotective effect in the neonatal mouse hypoxic-ischemic brain injury model of stroke. In addition, Tat-NR2B9c reduced brain damage caused by hypoxic-ischemic injury and showed the potential to promote long-term recovery. Tat-NR2B9c would be effective in treating or preventing perinatal and neonatal hypoxic-ischemic brain injury, as well as its related brain disorders. |
| 产品描述 | Tat-NR2B9cis designed to prevent nitric oxide (NO) production by preventing postsynaptic density protein 95 (PSD-95) binding to N-methyl-D-aspartate (NMDA) receptors and neuronal nitric oxide synthase.Tat-NR2B9cdissociates NMDA glutamate receptors from downstream excitotoxic signaling pathways without affecting normal glutamate receptor function. Neuroprotective effects ofTat-NR2B9chave been demonstrated in a diverse range of stroke models in several species including rodents, primates, and humans. Moreover,Tat-NR2B9cpeptide has shown clinical efficacy as a neuroprotective agent in acute stroke.[1][2] In vitro study indicated thatTat-NR2B9chave no measurable effect on the rate or magnitude of NMDA-induced calcium influx. However,Tat-NR2B9cprevented NMDA-induced DNA breaks, and the neuronal death could be significantly reduced byTat-NR2B9c.Tat-NR2B9calso prevented NMDA-induced superoxide p47phox formation by blocking phosphorylation, and neuroprotective effect ofTat-NR2B9cmay be partly or wholly attributable to its suppression of NOX2 activation. In addition,Tat-NR2B9c, which targets the PDZ domain of PSD-95, disrupts the functional coupling between NR2B and NOX2.[2] In vivo experiments demonstrated thatTat-NR2B9cwould be effective in treating or preventing perinatal and neonatal hypoxic-ischemic brain injury, as well as its related brain disorders. Results indicated thatTat-NR2B9creduced brain damage caused by hypoxic-ischemic injury when administered either before or after ischemia and improved post-HI neurobehavioral outcomes when delivered before or after ischemia. Moreover,Tat-NR2B9cmight exert neuroprotective effects through the promotion of pro-survival signaling and inhibition of pro-apoptotic signaling.[1] References: |
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