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Mangiferin activates the nuclear factor erythroid 2-related factor pathway to protect SOD1-G93A induced NSC-34 motor
Boyang Su1,2, Zhengqing He3, Jing Liu4
1Medical School of Chinese PLA, Beijing, China.
Abstract:
One of the main factors in the pathophysiology of amyotrophic lateral sclerosis is oxidative stress. Mangiferin (MF), a natural plant polyphenol, has anti-inflammatory and antioxidant effects. The aim of our study was to investigate the protective effects and mechanisms of MF in the hSOD1-G93A ALS cell model. Our result revealed that MF treatment reduced the generation of reactive oxygen species (ROS) and malondialdehyde (MDA), decreased oxidative damage, and reduced apoptosis. Additionally, it was observed that MF significantly increased the synthesis of the antioxidant genes hemeoxygenase-1 and NAD(P)H: quinone oxidoreductase 1, which are downstream of the Nrf2 signaling pathway, and increased the expression and activation of nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 knockdown greatly promoted apoptosis, which was reversed by MF treatment. To summarize, MF promoted the Nrf2 pathway and scavenged MDA and ROS to protect the ALS cell model.
Insights
Mangiferin (MF) protects against amyotrophic lateral sclerosis (ALS) by reducing oxidative stress and apoptosis. This natural polyphenol activates the Nrf2 pathway, enhancing antioxidant defenses in ALS cell models.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Oxidative stress is a key factor in amyotrophic lateral sclerosis (ALS) pathophysiology.
- Mangiferin (MF), a plant polyphenol, exhibits anti-inflammatory and antioxidant properties.
- Investigating MF's protective effects in ALS models is crucial for therapeutic development.
Purpose of the Study:
- To evaluate the protective effects and underlying mechanisms of Mangiferin (MF) in a cellular model of amyotrophic lateral sclerosis (ALS).
- To determine if MF can mitigate oxidative damage and apoptosis in the hSOD1-G93A ALS cell model.
Main Methods:
- Utilized the hSOD1-G93A cell model for amyotrophic lateral sclerosis (ALS).
- Assessed reactive oxygen species (ROS) and malondialdehyde (MDA) levels.
- Measured apoptosis, hemeoxygenase-1, and NAD(P)H: quinone oxidoreductase 1 gene expression.
- Investigated the Nrf2 signaling pathway, including Nrf2 expression, activation, and knockdown effects.
Main Results:
- Mangiferin (MF) treatment significantly reduced reactive oxygen species (ROS) and malondialdehyde (MDA) generation.
- MF decreased oxidative damage and inhibited apoptosis in the ALS cell model.
- MF treatment upregulated antioxidant genes (hemeoxygenase-1, NAD(P)H: quinone oxidoreductase 1) via the Nrf2 pathway.
- MF increased Nrf2 expression and activation, and its protective effects were confirmed even after Nrf2 knockdown.
Conclusions:
- Mangiferin (MF) demonstrates significant neuroprotective effects in an ALS cell model.
- MF exerts its protective action by scavenging ROS and MDA, and by activating the Nrf2 antioxidant pathway.
- MF holds potential as a therapeutic agent for managing oxidative stress in amyotrophic lateral sclerosis (ALS).
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