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Creative Biolabs

MPP⁺ Neuronal Cell Death Assay Service

Advance your Parkinson's disease (PD) research with our efficient and accurate MPP+-induced neuronal cell death detection solutions. We empower researchers to gain deeper insights into the disease's pathogenesis and accelerate the screening of potential therapeutic drugs. For further information regarding the products and services provided, project-specific consultation, and pricing, please submit an inquiry here.

Introduction

Distributed under Open Access license CC BY-SA 4.0, from Wiki, without modification.

MPP+ (1-methyl-4-phenylpyridinium ion) is a metabolite of MPTP (1-methyl-4-phenyl-2,3,6,7-tetrahydropyridine) and an important neurotoxin in PD research. It mainly enters dopaminergic neurons through the dopamine transporter (DAT) and accumulates inside the cells, inhibiting the mitochondrial electron transport chain complex I, leading to ATP depletion, increased production of reactive oxygen species (ROS), and cell death. In addition, MPP+ also induces the death of dopaminergic neurons through the combined action of oxidative stress and specific neurotoxins.

Our MPP+ Neuronal Cell Death Assays

  • Advanced Modeling System

Human iPSC-derived Neurons: Utilizing human induced pluripotent stem cell (iPSC)-derived neurons to create more physiologically relevant models and study the impact of genetic variability on MPP+ toxicity.

Co-culture Systems: Incorporating multiple cell types, such as astrocytes and microglia, to recreate the complex cellular environment of the brain and study cell-cell interactions in neurotoxicity.

Controllable Conditions: Our MPP+-induced neuronal cell death platform offers unparalleled control over experimental conditions. By manipulating key environmental factors, we can distinguish between apoptotic and non-apoptotic cell death modes, providing critical insights for developing targeted therapies.

Fig.1 Representative images of primary mouse cortical tri-culture. (Creative Biolabs Original) Fig.1 Representative images of primary mouse cortical tri-culture, NeuN (neuronal marker), GFAP (astrocyte marker) and Iba1 (microglia marker). Images acquired using Zeiss LSM 980.

  • Comprehensive Detection Indicators

Cell Viability and Morphology: Quantify cell survival rates and apoptotic features using MTT assays and Hoechst/PI double staining, precisely reflecting neuronal damage across MPP⁺ concentration gradients.

Mitochondrial Dysfunction: Assess mitochondrial health by measuring ROS levels, cytochrome c release, and changes in mitochondrial membrane potential, key indicators of mitochondrial dysfunction.

Programmed Cell Death Pathways: Investigate the activation of key cell death pathways, including Caspase-3 activation (apoptosis), AIF nuclear translocation (caspase-independent apoptosis), and LC3-II accumulation (autophagy).

Calcium Signaling Dysregulation: Monitor MPP+-induced Ca2+ overload and its association with lysosomal dysfunction using fluorescent probes, revealing the interplay between calcium signaling and neurodegeneration.

Fig.2 Intracellular reactive oxygen species fluorescence detection. Fig.2 Fluorescence detection of intracellular reactive oxygen species.1

  • High Throughput Detection Platform

Our MPP+-induced neuronal cell death platform is optimized for high-throughput screening, enabling researchers to efficiently evaluate the effects of multiple compounds on neurodegeneration. We support both 96-well and 384-well plate formats, allowing for rapid and cost-effective screening of large compound libraries.

Our MPP+ neuronal cell death assay service is your trusted partner in the fight against neurodegeneration. We provide comprehensive support, cutting-edge technology, and expert analysis to accelerate your research and drive the development of innovative therapies. Please contact us and let us work together.

Reference

  1. Lu, Xi-Lin, et al. "Paeonolum protects against MPP+-induced neurotoxicity in zebrafish and PC12 cells." BMC Complementary and Alternative Medicine 15 (2015): 1-10. Distributed under Open Access license CC BY 4.0, without modification.
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