包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
10mg | 电议 |
50mg | 电议 |
Cell lines | Primary cortical neuron(PCN) |
Preparation Method | PCNs were treated with Mdivi-1 (from 0.001 nM to 1 mM) dissolved in 0.1% DMSO 1 h before scratch cell injury. The release of lactate dehydrogenase(LDH)into the culture media was measured 6 h after scratch cell injury. |
Reaction Conditions | 0.001 nM to 1 mM for 1hour |
Applications | Using LDH assay, exposing PCNs to scratch cell injury with Mdivi-1 (100 μM and 1 mM) resulted in significant dose-dependent inhibition of cell death. Hence the range of the optimum concentration was from 10 μM to 100 μM. |
Animal models | male ICR mice |
Preparation Method | For the mice treated with Mdivi-1 (3 mg/kg), dynamin-related protein 1 (Drp1) inhibitor, was administered by intraperitoneal injection 10 min after TBI. Mdivi-1 was dissolved in 0.01 M PBS. Vehicle animals received an intraperitoneal injection of 0.01 M PBS. |
Dosage form | Intraperitoneal injection, 3 mg/kg |
Applications | Treatment with Mdivi-1 accelerated the recovery of motor functional outcome on days 3-5 post-TBI. After injury, animals subjected to Mdivi-1 treatment demonstrated a significant decrease in the latencies, relative to vehicle mice on days 15 and 16, thereby Mdivi-1 treatment could result in cognitive functional recovery. |
产品描述 | Mdivi-1 (Mitochondrial division inhibitor 1) inhibits traumatic brain injury (TBI)-induced dynamin-related protein 1(Drp1) up-regulation, autophagy dysfunction and mitophagy activation. Mdivi-1 decreased TBI-induced cell death and lesion volume[1,2]. Mdivi-1 is a selective Drp 1 inhibitor with IC50 value as 10 mμ[3]. Mdivi-1 significantly alleviated the scratch injury-induced cell death, loss of mitochondrial membrane potential, reactive oxygen species (ROS) production and ATP reduction in primary cortical neurons (PCNs). Additionally, the lysosome inhibitor chloroquine (CQ) abrogated the Mdivi-1-induced decrease in autophagosomes accumulation and cell death at 24 h both in the basal state and under the conditions of scratch cell injury[1]. Mdivi-1 could significantly rescue neurons from death induced by seizures in a dose-dependent manner. In addition, the seizures increase Drp1 expression in hippocampus. These suggested that the up-regulation of Drp1 expression could be partially responsible for seizure-induced neuronal death. Moreover, CytC release, AIF translocation and caspase-3 activation may be involved in the protective mechanisms of mdivi-1 against seizure-induced neuronal death[4]. References: |