| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 5mg | 电议 |
| 10mg | 电议 |
| 25mg | 电议 |
| 50mg | 电议 |
Cell lines | The human neuroblastoma cell line SH-SY5Y |
Preparation Method | Cells were cultured in RPMI-1640 supplemented with 10% FBS at 37 °C. Cells at 60-70% confluence were treated with concentrations of Aβ25-35, Methyllycaconitine citrate, rapamycin or Aβ25 35 with or without Methyllycaconitine citrate. |
Reaction Conditions | 2.5-20uM Methyllycaconitine citratefor 24h |
Applications | Pretreatment with 5 and 10 uM Methyllycaconitine citrate inhibited the decreased cell viability induced by Aβ25-35, which suggested that MLA had a protective effect against Aβ-induced cytotoxicity. Furthermore, cell viability did not decrease after exposure to Methyllycaconitine citrate (2.5, 5, 10, 20 uM), which suggests a good safety profile |
Animal models | White Swiss-Webster male mice |
Preparation Method | Mice were initially injected with primary injection solution (0.2 mL) for a dose of 50 µg of hapten fetuin conjugate( Methyllycaconitine citrate and MLA-BSA). Booster injections (0.2 mL) with the same dose of hapten fetuin conjugate in incomplete Freund's adjuvant were given at 3-wk intervals. Control mice were initially injected s.c. with control primary injection solution. At the same time, the treated mice received booster injections the control mice were given control booster injections (0.2 mL). |
Dosage form | 1 mg/mL Methyllycaconitine citrate 0.2ML |
Applications | Vaccination altered Methyllycaconitine citrate toxicity in mice and that vaccination may be useful in decreasing the effects of larkspur toxins in animals. |
| 产品描述 | Methyllycaconitine citrate (MLA), a norditerpenoid alkaloid isolated from the seeds of Delphinium brownie. Methyllycaconitine citrate (MLA) is an antagonist of α7-containing neuronal nicotinic acetylcholine receptors (α7nAChR)[2]. Pretreatment with 5 and 10 uM MLA inhibited the decreased cell viability induced by Aβ25-35, which suggested that MLA had a protective effect against Aβ-induced cytotoxicity. Furthermore, cell viability did not decrease after exposure to MLA (2.5, 5, 10, 20 uM), which suggests a good safety profile[1].Because of Methyllycaconitine citrate (MLA) is specific, concentration-dependent, reversible, and voltage-independent antagonism, it could inhibit acetylcholine- and anatoxin-induced whole-cell currents in cultured fetal rat hippocampal neurons[3]. When test the influence of Methyllycaconitine citrate on acute METH effects and neurotoxicity in mice, using both in vivo and in vitro models. MLA inhibited METH-induced climbing behavior by 50%. Acute effects after 30-min preincubation with 1μM METH also included a decrease in striatal synaptosome dopamine (DA) uptake, which was prevented by MLA. METH-induced neurotoxicity was assessed in vivo in terms of loss of striatal dopaminergic terminals (73%) and of tyrosine hydroxylase levels (by 90%) at 72 h post-treatment, which was significantly attenuated by MLA[4]. 50 nM Methyllycaconitine citrate partially inhibited (by 16%) [(3)H]dopamine release from rat striatal synaptosomes stimulated with 10 microM nicotine. Other alpha7-selective antagonists had no effect. Similarly, Methyllycaconitine citrate (50 nM) inhibited [(3)H]dopamine release evoked by the partial agonist (2-chloro-5-pyridyl)-9-azabicyclo[4.2.1]non-2-ene (UB-165) (0.2 microM) by 37%[5]. Methyllycaconitine citrate was administered to animals allowed to self-administer nicotine intravenously, and also to animals that had been prepared with nicotine-containing osmotic mini-pumps and trained on a brain stimulation reward procedure. The results indicated that pretreatment with the highest doses of MLA used (3.9 and 7.8 mg/kg) significantly reduced nicotine self-administration at two doses of self-administered nicotine (0.03 and 0.06 mg/kg/infusion)[6]. Vaccination altered methyllycaconitine toxicity in mice and that vaccination may be useful in decreasing the effects of larkspur toxins in animals[7]. References: |
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