Mitochondrial
dysfunction is an expected cause of etiology and progression in
numerous human neurological pathologies, including stroke, Alzheimer's,
and Parkinson's diseases. Therefore, a neuroprotective treatment is an
urgent and unmet need. Transition metal dichalcogenide nanoflowers (TMD
NFs) exhibit unique biological properties. However, neuroprotective
properties of these nanomaterials remain poorly understood. In the
current study, the biological effect of molybdenum disulfide and
molybdenum diselenide TMD NFs on neurons and astrocytes was
investigated. It was found that both nanomaterials lowered reactive
oxygen species levels, reduced mitochondrial impairment, and increased
mitochondrial biogenesis. Neuroprotective effects of both TMD NFs
resulted from upregulation of the peroxisome proliferator-activated
receptor gamma coactivator 1 alpha pathway, the biological system
responsible for mitochondrial biogenesis. Furthermore, administration of
TMD NFs to Caenorhabditis elegans extended lifespan of the
nematodes. These results indicate that TMD NFs can be used as novel
neuroprotective therapeutic agents against acute and chronic
neurological condition linked to mitochondrial dysfunction.
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