Protective effects of Marine Sponge Extract MS01 on Neuronal Cell Lines

Authors

  • G.B. Priyadharshini, C. Jaynthy

DOI:

https://doi.org/10.53555/jaz.v44iS2.2420

Keywords:

Reactive oxygen species, Marine sponges, Flow cytometry, cell degradation, Neuroprotection, and cell lines

Abstract

Reactive oxygen species (ROS), byproducts of aerobic respiration, play a crucial role in cellular signal transduction. However, excessive ROS production can lead to cell death by damaging DNA, proteins, and lipids. Neuroprotection, a defensive mechanism that mitigates cell degeneration and initiates cell regeneration, can be facilitated by bioactive proteins and other substances abundant in marine sponges. In this study, we employed flow cytometry to investigate the protective effects of the sponge extract MS01 against ROS in fibroblast cell lines (L929) as well as human neuronal cell lines (HMC3 and U251).

Results: Our findings indicate that MS01 exhibits notable AChE inhibitory activity, with an IC50 value of 265.13 µg/ml. Furthermore, assessments conducted on the human malignant glioma cell line and human microglial clone 3 revealed no potential for cell death, demonstrating the non-toxic nature of the extract. Flow cytometry analysis using FITC antibody in L929 cells demonstrated a reduction in iNOS activity with a mean fluorescent intensity of 62.12 MFI, indicating therapeutic potential. Moreover, MS01 significantly decreased H2DCFDA fluorescence expression in H2O2-treated cells, indicating its protective properties.

Conclusion: The results of this study show that MS01, an extract obtained from marine sponges, appears promising for the treatment for neurodegeneration. The findings demonstrate that MS01 has characteristics that may reduce acetylcholinesterase activity, scavenge nitric oxide radicals, and efficiently suppress reactive oxygen species. The test compound additionally demonstrated no evidence of causing apoptosis or toxicity in healthy brain cells, confirming its potential therapeutic utility. 

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Published

2023-11-30

Issue

Section

Articles

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