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The Impact of Fucoxanthin on Oxidative Stress Damage in Human Placenta-Derived Mesenchymal Stem Cells: Insights from the PI3K/Akt/Nrf-2 Pathway

The Impact of Fucoxanthin on Oxidative Stress Damage in Human Placenta-Derived Mesenchymal Stem Cells: Insights from the PI3K/Akt/Nrf-2 Pathway

Introduction:
Oxidative stress is a condition that occurs when there is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them or repair the resulting damage. It has been implicated in various diseases, including cancer, cardiovascular diseases, and neurodegenerative disorders. Human placenta-derived mesenchymal stem cells (hPMSCs) have shown promising potential in regenerative medicine due to their ability to differentiate into various cell types and their immunomodulatory properties. However, oxidative stress can impair the therapeutic efficacy of hPMSCs. In recent years, researchers have been exploring natural compounds that can protect hPMSCs from oxidative stress damage. One such compound is fucoxanthin, a carotenoid found in brown seaweed. This article aims to explore the impact of fucoxanthin on oxidative stress damage in hPMSCs and shed light on the underlying mechanisms involving the PI3K/Akt/Nrf-2 pathway.

Fucoxanthin and its Antioxidant Properties:
Fucoxanthin has gained attention for its potent antioxidant properties. It is known to scavenge free radicals and inhibit lipid peroxidation, a process that damages cell membranes. Several studies have demonstrated the ability of fucoxanthin to protect various cell types from oxidative stress-induced damage. However, its impact on hPMSCs and the mechanisms involved are still being investigated.

The PI3K/Akt/Nrf-2 Pathway:
The PI3K/Akt/Nrf-2 pathway plays a crucial role in cellular defense against oxidative stress. Phosphoinositide 3-kinase (PI3K) activates Akt, which in turn phosphorylates and activates nuclear factor erythroid 2-related factor 2 (Nrf-2). Nrf-2 translocates to the nucleus and binds to antioxidant response elements (AREs) in the DNA, leading to the upregulation of various antioxidant enzymes and proteins. Activation of this pathway can enhance the cellular antioxidant defense system and protect against oxidative stress damage.

Impact of Fucoxanthin on hPMSCs:
Recent studies have shown that fucoxanthin can protect hPMSCs from oxidative stress-induced damage. In one study, hPMSCs were pretreated with fucoxanthin before exposure to hydrogen peroxide, a potent inducer of oxidative stress. The results showed that fucoxanthin significantly reduced ROS levels and lipid peroxidation in hPMSCs. Moreover, fucoxanthin increased the expression of antioxidant enzymes, such as superoxide dismutase (SOD) and catalase, through the activation of the PI3K/Akt/Nrf-2 pathway. These findings suggest that fucoxanthin can enhance the antioxidant defense system in hPMSCs and protect them from oxidative stress damage.

Insights from the PI3K/Akt/Nrf-2 Pathway:
Further investigations into the underlying mechanisms revealed that fucoxanthin activates the PI3K/Akt/Nrf-2 pathway in hPMSCs. Activation of this pathway leads to the translocation of Nrf-2 into the nucleus, where it binds to AREs and upregulates the expression of antioxidant enzymes. Fucoxanthin-mediated activation of this pathway also increased the expression of heme oxygenase-1 (HO-1), an enzyme involved in cellular defense against oxidative stress. Additionally, fucoxanthin was found to inhibit the activation of nuclear factor-kappa B (NF-κB), a transcription factor involved in inflammation and oxidative stress. This dual action of fucoxanthin on the PI3K/Akt/Nrf-2 pathway and NF-κB suggests its potential as a therapeutic agent for oxidative stress-related diseases.

Conclusion:
Oxidative stress can impair the therapeutic efficacy of hPMSCs, limiting their potential in regenerative medicine. Fucoxanthin, a natural compound found in brown seaweed, has shown promising antioxidant properties and the ability to protect hPMSCs from oxidative stress-induced damage. The activation of the PI3K/Akt/Nrf-2 pathway and inhibition of NF-κB by fucoxanthin contribute to its protective effects. Further research is needed to fully understand the mechanisms involved and explore the potential of fucoxanthin as a therapeutic agent for oxidative stress-related diseases. Nonetheless, these findings provide valuable insights into the impact of fucoxanthin on hPMSCs and highlight its potential in regenerative medicine.

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