Ebselen, Iron Uptake Inhibitor, Alleviates Iron Overload-Induced Senescence-Like Neuronal Cells SH-SY5Y via Suppressing the mTORC1 Signaling Pathway.

Increasing evidence highlights that excessive iron accumulation in the brain plays a vital role in neuronal senescence and is implicated in the pathogenesis of age-related neurodegenerative diseases, including Alzheimer's disease (AD) and Parkinson's disease (PD). Therefore, the chemical compounds that eliminate an iron overload may provide better protection against oxidative stress conditions that cause the accumulation of senescent cells during brain aging. Ebselen has been identified as a strongly useful compound in the research on redox biology mechanisms.

Characterization, expression and function of the pyrokinins (PKs) in the giant freshwater prawn, Macrobrachium rosenbergii.

Pyrokinins (PKs) are neuropeptides that have been found to regulate a variety of physiological activities including reproduction in various insect and crustacean species. However, the reproductive roles of PKs in the giant freshwater prawn, Macrobrachium rosenbergii, have not yet been investigated. In this study, we identified the MroPK gene from next-generation sequence resources, which encodes a MroPK precursor that shares a high degree of conservation with the C-terminal sequence of FxPRLamide in other arthropods.

Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells.

The generation of excessive mitochondrial reactive oxygen species (mtROS) is associated with glutamate-stimulated neurotoxicity and pathogenesis of Alzheimer's disease (AD). Impaired mitochondrial function is accompanied with oxidative stress that is a significant contributor to initiate autophagy, but the underlying mechanisms are not fully understood. The present study aimed to investigate the neuroprotective effects of Mito-Tempo on glutamate-induced neuroblastoma SH-SY5Y cell toxicity.

Effects of alcohol administration during adulthood on parvalbumin and glial fibrillary acidic protein immunoreactivity in the rat cerebral cortex.

The pathology of brain atrophy mediated by alcohol was investigated in all parts of the cerebral cortex (the frontal, parietal, temporal lobes and occipital cortex) by using two markers: parvalbumin (PV) and glial fibrillary acidic protein (GFAP). Three-month old male Wistar rats were divided into control (C) and alcohol-exposed groups. The control group received distilled water, whereas the alcohol-exposed groups received either a low dose (2g/kg body wt) or a high dose (5g/kg) of ethanol for periods of 21 days, 3 or 6 months.

Alcohol administration during adulthood induces alterations of parvalbumin and glial fibrillary acidic protein immunoreactivity in rat hippocampus and cingulate cortex.

Alcohol induces impairment of cognition, learning and memory. Neurotoxic effects of alcohol on the pathology of the hippocampus and the cingulate cortex were investigated in experimental rats. Parvalbumin (PV), a calcium-binding protein, is a crucial component of GABAergic neurons and glial fibrillary acidic protein immunoreactive (GFAP-ir) astrocytes have been used as markers.