MPP+ Iodide
(Synonyms: 1-甲基-4-苯基吡啶鎓碘化物) 目录号 : GC18188
MPP+ Iodide(1-methyl-4-phenylpyridinium iodide)是神经毒素 MPTP 的一种有毒代谢物,通过选择性破坏黑质中的多巴胺能神经元,在体外模型中成功诱导了帕金森样综合征。
Cas No.:36913-39-0
Sample solution is provided at 25 µL, 10mM.
MPP+ Iodide (1-methyl-4-phenylpyridinium?iodide) is a toxic metabolite of the neurotoxin MPTP, and has successfully induced Parkinson-like syndromes in an in vitro model by selectively destroying dopaminergic neurons in substantia nigra.[1]
In vitro efficacy test it shown that when SH-SY5Y cells were exposed to MPP+ Iodidein the range of 1–100 M for 3–24 h, MPP+ Iodide exhibited a dose-time dependent cytotoxicity.[1] In vitro experiment it indicated that SH-SY5Y cells were treated with 0.2, 0.4, 0.8, or 1.0 mM MPP?+ for 24 h, MPP+ Iodide?could significantly reduce cell viability in a dose-dependent manner.[2] In vitro, treatment with 1-7.5 mM of MPP+ Iodide dose-dependently increased the neurodegeneration in the L1 larvae of BZ555 worms. The percentages of worms exhibiting neurodegeneration after treatment with 1 mM, 2.5 mM, 5 mM and 7.5 mM MPP+ Iodide were 24%, 27%, 67% and 87%, respectively.[3] Both TSM1 and primary neurons were treated with 0.1 to 2 mM of MPP+ Iodide induced neuronal cell death in a concentration dependent manner in vitro. TSM1 cells and primary neurons were treated with 400 μM MPP+ Iodide decreased by 60% and 80% the cell viability as compared to the control, respectively.[4] In vitro to test the role of MAC1 in MPTP/MPP+-induced neurotoxicity, neuron-glia cultures were treated with 0.125, 0.25, or 0.5 μM of MPP+ Iodidefound that MPP+-induced DAergic neurotoxicity in neuron-glia cultures was attenuated in the absence of MAC1.[5]
In vivo study indicated that intranigral infusion of 3 μg/μl MPP+ Iodideinduced oxidative injury in nigrostriatal dopaminergic system of rat brain; and autophagy is pro-death in the MPP+-induced oxidative injury.[6]
References:
[1].Reudhabibadh R, et al. Suppressing Cdk5 Activity by Luteolin Inhibits MPP+-Induced Apoptotic of Neuroblastoma through Erk/Drp1 and Fak/Akt/GSK3β Pathways. Molecules. 2021 Feb 28;26(5):1307.
[2].Yan J, et al. Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells. J Biol Res (Thessalon). 2021 Feb 25;28(1):6.
[3].Anjaneyulu J, et al. Differential effect of Ayurvedic nootropics on C.?elegans models of Parkinson's disease. J Ayurveda Integr Med. 2020 Oct-Dec;11(4):440-447.
[4].Petit-Paitel A, et al. Involvment of cytosolic and mitochondrial GSK-3beta in mitochondrial dysfunction and neuronal cell death of MPTP/MPP-treated neurons. PLoS One. 2009;4(5):e5491.
[5].Hu X, et al. Macrophage antigen complex-1 mediates reactive microgliosis and progressive dopaminergic neurodegeneration in the MPTP model of Parkinson's disease. J Immunol. 2008 Nov 15;181(10):7194-204.
[6].Hung KC, et al. Roles of autophagy in MPP+-induced neurotoxicity in vivo: the involvement of mitochondria and α-synuclein aggregation. PLoS One. 2014 Mar 19;9(3):e91074.
MPP+ Iodide(1-methyl-4-phenylpyridinium iodide)是神经毒素 MPTP 的一种有毒代谢物,通过选择性破坏黑质中的多巴胺能神经元,在体外模型中成功诱导了帕金森样综合征。[ 1]
体外药效试验表明,当 SH-SY5Y 细胞暴露于 1-100 M 范围内的 MPP+ 碘化物 3-24 小时时,MPP+ 碘化物表现出剂量时间依赖性细胞毒性。[1]< /sup> 体外实验表明,SH-SY5Y 细胞用 0.2、0.4、0.8 或 1.0 mM MPP + 处理 24 h,MPP+ Iodide〉 可以剂量依赖性方式显着降低细胞活力。[2 ] 在体外,用 1-7.5 mM 的 MPP+ 碘化物处理会剂量依赖性地增加 BZ555 蠕虫 L1 幼虫的神经变性。用 1 mM、2.5 mM、5 mM 和 7.5 mM MPP+ 碘化物处理后表现出神经变性的蠕虫百分比分别为 24%、27%、67% 和 87%。[3] TSM1 和用 0.1 至 2 mM 的 MPP+ 碘化物处理初级神经元,在体外以浓度依赖性方式诱导神经元细胞死亡。 TSM1 细胞和原代神经元用 400 μM MPP+ 碘化物处理,与对照相比,细胞活力分别降低了 60% 和 80%。[4] 在体外测试 MAC1 在 MPTP 中的作用/MPP+- 诱导的神经毒性,神经胶质培养物用 0.125、0.25 或 0.5 μM 的 MPP+ 碘化物处理,发现在没有 MAC1 的情况下,MPP+- 诱导的神经胶质培养物中的 DAergic 神经毒性减弱。[5]/ p>\n
体内研究表明,黑质内输注 3 μg/μl MPP+ 碘化物可诱导大鼠大脑黑质纹状体多巴胺能系统的氧化损伤;在 MPP+- 诱导的氧化损伤中,自噬促进死亡。[6]
Cell experiment [1]: | |
Cell lines |
Bv-2 cells |
Preparation Method |
The cell experiment took Bv-2 cells as the object, set the MPP+ Iodidefinal concentration of 0.1, 0.2, 0.5 mmol as the interference concentration, and after 24 h of culture, Western blot detected the expression level of NLRP3 protein in cells, and selected the optimal concentration. |
Reaction Conditions |
0.1, 0.2, 0.5 mmol, 24h |
Applications |
After 0.1/0.2/0.5 mmol MPP+ Iodide intervention cells for 24 h, MPP+ Iodideactivated cells expressed NLRP3 and MIF protein significantly higher than in the control group. 0.2 mmol MPP+ Iodideis the optimal concentration of NLRP3 inflammasomes that activate Bv-2. |
Animal experiment [2]: | |
Animal models |
Male Sprague–Dawley rats |
Preparation Method |
Four days after siRNA infusion, rats were re-anesthetized for intranigral infusion of MPP+ Iodide(3 µg/µl) at a rate of 0.2 µl/min. After the surgery, rats recovered from anesthesia and were placed in home cages for the indicated times. |
Dosage form |
3 µg/µl;intranigral infusion |
Applications |
The results shown intranigral infusion of MPP+ Iodideincreased HO-1 levels in a time-dependent manner; significant HO-1 elevation was observed 24 h to 7 d after MPP+ Iodideinfusion. |
References: [1]. Huang H, et al. [Macrophage migration inhibitory factor meditates MPP+/MPTP-induced NLRP3 inflammasome activation in microglia cells]. Nan Fang Yi Ke Da Xue Xue Bao. 2021 Jul 20;41(7):972-979. Chinese. [2]. Hung KC, et al. Roles of autophagy in MPP+-induced neurotoxicity in vivo: the involvement of mitochondria and α-synuclein aggregation. PLoS One. 2014 Mar 19;9(3):e91074. |
Cas No. | 36913-39-0 | SDF | |
别名 | 1-甲基-4-苯基吡啶鎓碘化物 | ||
化学名 | 1-methyl-4-phenyl-pyridinium, monoiodide | ||
Canonical SMILES | C[N+](C=C1)=CC=C1C2=CC=CC=C2.[I-] | ||
分子式 | C12H12N.I | 分子量 | 297.1 |
溶解度 | 100 mM in Water | 储存条件 | Store at RT |
General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
||
Shipping Condition | 评估样品解决方案:配备蓝冰进行发货。所有其他可用尺寸:配备RT,或根据请求配备蓝冰。 |
制备储备液 | |||
![]() |
1 mg | 5 mg | 10 mg |
1 mM | 3.3659 mL | 16.8294 mL | 33.6587 mL |
5 mM | 0.6732 mL | 3.3659 mL | 6.7317 mL |
10 mM | 0.3366 mL | 1.6829 mL | 3.3659 mL |
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
第二步:请输入动物体内配方组成(配方适用于不溶于水的药物;不同批次药物配方比例不同,请联系GLPBIO为您提供正确的澄清溶液配方) | ||||||||||
% DMSO % % Tween 80 % saline | ||||||||||
计算重置 |
计算结果:
工作液浓度: mg/ml;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
-
Related Biological Data
Nicotine treatment mitigates MPP+- induced apoptosis in HEK293T cells.d The bright field and live/dead staining images of different treatment groups.
Group 1, normal control; group 2, nicotine treatment group; group 3, nicotine + MPP+ treatment group (nicotine was added 4 h before MPP+ treatment); and group 4, MPP+(GlpBio) treatment group. After incubation for 24 h, the cells were washed and incubated with calcein AM and propidium iodide for 30 min.
J Transl Med 22.1 (2024): 1-21. PMID: PMID: 38609979 IF: 7.4001 -
Related Biological Data
Neuroprotective activity of novel natural compounds from marine coral.(C, D) The cell viability of SH-SY5Ycells treated with compounds from the primary screening and MPP+ (500 μM) or H2O2 (100 μM).
SH-SY5Y cell damage models were successfully established by 500 μM MPP+ (Glpbio)or 100 μM H2O2.
CNS Neuroscience & Therapeutics (2022). PMID: 36419251 IF: 7.0348