Abstract
Reactive oxygen species are well known for induction of oxidative stress conditions through oxidation of vital biomarkers leading to cellular death via apoptosis and other process, thereby causing devastative effects on the host organs. This effect is believed to be linked with pathological alterations seen in several neurodegenerative disease conditions. Many phytochemical compounds proved to have robust antioxidant activities that deterred cells against cytotoxic stress environment, thus protect apoptotic cell death. In view of that we studied the potential of glucomoringin-isothiocyanate (GMG-ITC) or moringin to mitigate the process that lead to neurodegeneration in various ways. Neuroprotective effect of GMG-ITC was performed on retinoic acid (RA) induced differentiated neuroblastoma cells (SHSY5Y) via cell viability assay, flow cytometry analysis and fluorescence microscopy by means of acridine orange and propidium iodide double staining, to evaluate the anti-apoptotic activity and morphology conservation ability of the compound. Additionally, neurite surface integrity and ultrastructural analysis were carried out by means of scanning and transmission electron microscopy to assess the orientation of surface and internal features of the treated neuronal cells. GMG-ITC pre-treated neuron cells showed significant resistance to H2O2-induced apoptotic cell death, revealing high level of protection by the compound. Increase of intracellular oxidative stress induced by H2O2 was mitigated by GMG-ITC. Thus, pre-treatment with the compound conferred significant protection to cytoskeleton and cytoplasmic inclusion coupled with conservation of surface morphological features and general integrity of neuronal cells. Therefore, the collective findings in the presence study indicated the potentials of GMG-ITC to protect the integrity of neuron cells against induced oxidative-stress related cytotoxic processes, the hallmark of neurodegenerative diseases.
Highlights
Reactive oxygen species (ROS) including hydrogen peroxide (H2O2) are known by their induction of oxidative stress believed to be linked with various neurodegenerative disease (NDD) conditions including but not limited to amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Parkinson’s diseases (PD) [1,2]
To demonstrate the transformation of SHSY5Y cells into neuronal lineage used in the present study, the 10 μM retinoic acid (RA) treated cells with extended neurites was observed after 24 hours of treatment
Undifferentiated cells revealed no or comparatively smaller neurites (Fig 1b), indicating that the SHSY5Y cells were differentiated in to typical neuronal cells they were used throughout the experimental analyses
Summary
Reactive oxygen species (ROS) including hydrogen peroxide (H2O2) are known by their induction of oxidative stress believed to be linked with various neurodegenerative disease (NDD) conditions including but not limited to amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD) and Parkinson’s diseases (PD) [1,2] It occurs through oxidation of vital cellular biomarkers such as nucleic acids and proteins, crosslinking of membrane constituent and lipids of all kinds within and outside cells [3,4,5]. Even though a number of cell types considered H2O2 mitogenic at low concentration [6], it is oxidizable effect at overwhelming quantity often leads to the general cellular damage with consequent death via apoptosis and other processes, affecting the host organs severely [7]. Apoptotic mechanism usually switches on to eliminate neurons deemed unbearable [12,13], resulting to severe morphological and functional deficit, leading to progressive decline in cognitive and memory well-being [14,15]
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