| CAS NO: | 23007-85-4 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 250mg | 电议 |
| 500mg | 电议 |
| Molecular Weight (MW) | 209.72 |
|---|---|
| Formula | C12H15N·HCl |
| CAS No. | 23007-85-4 |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: 20 mg/mL (95.4 mM) |
| Water: 41 mg/mL (195.5 mM) | |
| Ethanol: 41 mg/mL (195.5 mM) | |
| Solubility (In vivo) | CN1CC=C(C2=CC=CC=C2)CC1.[H]Cl |
| Synonyms | MPTP hydrochloride; MPTP HCl |
| In Vitro | In vitro activity: The morphology of N2AB-1 and glioma cells was unaltered when these cells were exposed to all doses of MPTP. And, C6 glioma cell proliferation was also unaffected by MPTP treatment. MPTP Promotes Apoptosis and Tau Phosphorylation in Human Neuroblastoma M17 Cells. MPTP significantly promotes Tau phosphorylation at Ser262 in human neuroblastoma M17 cells. MPTP caused a dose-dependent increase in the intracellular α-synuclein level in our M17 human neuroblastoma cells. MPTP appears to promote Tau phosphorylation in the brain by activating both PKA and GSK3β. Kinase Assay: MPTP inhibited the nerve-evoked twitches of phrenic nerve-hemidiaphragm preparations from ICR mice (20-30 g). PP 50 uM, but not PA 50 uM or TP 50 uM, potentiated the inhibitory effect of MPTP. PP 100 uM itself had an inhibitory action on twitch amplitude. The IC50 values for twitch inhibition by MPTP, TC and PP were 53, 0.7 and 123 uM, respectively. Pretreatment with PP 50 uM reduced the IC50 values of MPTP and TC to 18 and 0.3 uM, respectively. Cell Assay: N2AB-1 and C6 glioma cells were plated in 24-well costar dishes (16 mm diameter) at 50,000 cells per well with the culture medium described above. After 24 h medium was removed and medium with varying concentrations of MPTP or MPP+ was added in duplicate. Control and treated cells were then trypsinized and counted with a hemocytometer every day for 3 days following treatment. |
|---|---|
| In Vivo | The number of tyrosine hydroxylase-positive neurons was decreased in the substantia nigra pars compacta of MPTP-treated mice. MPTP decreased thioredoxin reductase 1 expression and thioredoxin reductase activity in the mouse midbrain, reduced the number of thioredoxin reductase 1-positive cells in the substantia nigra pars compacta of mice. Administration of the toxin MPTP can cause neurochemical, behavioral and histopathological alterations in human and nonhuman primates that are similar to those observed in Parkinsonian patients. Compared with primates, rodents are insensitive to MPTP. MPTP can be administered by various routes, such as gavage and stereotactic injection, but the most common and reproducible route is systemic administration, including subcutaneous, intravenous, intraperitoneal and intramuscular injection. MPTP is a lipophilic protoxin that can rapidly cross the blood-brain barrier following systemic injection. Once it enters the brain, MPTP is converted to 1-methyl-4-phenylpyridine by monoamine oxidase B. MPTP has been shown to be toxic to dopaminergic neurons of the nigrostriatal system in humans, monkeys, and mice and to produce long-lasting depletion of DA and its metabolites in the striatum. |
| Animal model | C57BL/6 mice |
| Formulation & Dosage | Dissolved in saline; 20 mg/kg; i.p. |
| References | Neural Regen Res. 2013 Dec 15;8(35):3275-83; Neurotoxicol Teratol. 2002 Sep-Oct;24(5):599-605; Brain Res. 1988 Jul 26;456(2):254-62; J Biol Chem. 2011 Feb 18;286(7):5055-68. |
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