This
Article summarizes the likely benefits of central nervous
system oxidative preconditioning in the reduction of COVID-19 based
on its putative pathogenesis. The current COVID-19 outbreak caused
a pandemic with millions of infected patients and death cases worldwide.
The clinical features of severe acute respiratory syndrome coronavirus
(SARS-CoV) was initially linked with respiratory disorders, but recent
studies have reported alterations of neurological and cerebrovascular
functions in COVID-19 patients. The main viral infection features
are related to cell death, inflammation, and cytokine generation,
which can be associated with the dysregulation of redox systems or
oxidative stress. However, until now, there is no available and effective
therapeutic approach. Thus, it is necessary to search for care and
adequate protection against the disease, especially for susceptible
and vulnerable groups. Preconditioning, a well-known antioxidative
stress and anti-inflammatory approach, is protective against many
neurological age-related disorders. COVID-19 severity and morbidity
have been observed in elderly patients. The aim of the present study
is to elucidate the possible protective role of oxidative preconditioning
in aged patients at high risk of developing severe COVID-19 complications.
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Activation of the apoptotic pathway has been associated with promoting neuronal cell death in the pathophysiology of Parkinson disease (PD). Nonetheless, the mechanisms by which it may occurs remain unclear. It has been suggested that stress-induced oxidation and potentially apoptosis may play a major role in the progression of PD. Thus, in this study, we aimed to investigate the effect of subchronic restraint stress on striatal dopaminergic activity, iron, p53, caspase-3, and plasmatic acetylcholinesterase (AChE) levels in an animal model of PD induced by administration of 6-hydroxydopamine(6-OHDA) in the medial forebrain bundle (MFB). The obtained results showed that restraint stress exacerbates motor coordination deficits and anxiety in animals treated with 6-OHDA in comparison to animals receiving saline, and it had no effect on object recognition memory. On another hand, 6-OHDA decreased dopamine(DA) levels, increased iron accumulation, and induced overexpression of the pro-apoptotic factors caspase-3, p53, and AChE. More interestingly, post-lesion restraint stress exacerbated the expression of caspase-3 and AChE without affecting p53 expression. These findings suggest that subchronic stress may accentuate apoptosis and may contribute to DA neuronal loss in the striatal regions and possibly exacerbate the progression of PD.
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