Empleo de indicadores bioquímicos en el estudio del estrés psicosocial laboral. Tendencias en la investigación / Use of biochemical indicators in the study of the psychosocial stress at work. Tendencies in the investigation

Las investigaciones sobre el estrés y la salud se caracterizan por un impresionante comportamiento ascendente, pero con un énfasis desproporcionado de investigaciones descriptivas en detrimento de las explicativas a niveles fisiológico, biológico y bioquímico. Se realizó una revisión de las tendencias actuales en el estudio del estrés, donde se emplearon indicadores bioquímicos. El término de carga alostática aparece con preeminencia -18 referencias, incluyendo del año 2014-. Se analizaron entre las múltiples respuestas hormonales al estrés, el papel de la hormona liberadora de córticotrofina, la vasopresina y citocinas proinflamatorias como marcadores bioquímicos de la cascada inflamatoria, específicamente las interleucinas 1 y 6 y el factor de crecimiento tumoral. Se argumenta por qué el síndrome de burnout, consecuencia del estrés laboral crónico, puede ser reconocido como un síndrome neuroendocrino de etiología conocida. Finalmente, se hace referencia a un estudio experimental en el cual el comportamiento es explicado empleando indicadores bioquímicos e introduciendo elementos de la biología molecular. Se concluye sobre la pertinencia de investigaciones multidisciplinarias y su alcance para abordar los problemas actuales de salud de la población trabajadora(AU)

C-Phycocyanin is neuroprotective against global cerebral ischemia/reperfusion injury in gerbils.

Although the huge economic and social impact and the predicted incidence increase, neuroprotection for ischemic stroke remains as a therapeutically empty niche. In the present study, we investigated the rationale of the C-Phycocyanin (C-PC) treatment on global cerebral ischemia/reperfusion (I/R) injury in gerbils. We demonstrated that C-PC given either prophylactically or therapeutically was able to significantly reduce the infarct volume as assessed by triphenyltetrazolium chloride (TTC) staining and the neurological deficit score 24h post-stroke. In addition, C-PC exhibited a protective effect against hippocampus neuronal cell death, and significantly improved the functional outcome (locomotor behavior) and gerbil survival after 7 days of reperfusion. Malondialdehyde (MDA), peroxidation potential (PP) and ferric reducing ability of plasma (FRAP) were assayed in serum and brain homogenates to evaluate the redox status 24h post-stroke. The treatment with C-PC prevented the lipid peroxidation and the increase of FRAP in both tissue compartments. These results suggest that the protective effects of C-PC are most likely due to its antioxidant activity, although its anti-inflammatory and immuno-modulatory properties reported elsewhere could also contribute to neuroprotection. To our knowledge, this is the first report of the neuroprotective effect of C-PC in an experimental model of global cerebral I/R damage, and strongly indicates that C-PC may represent a potential preventive and acute disease modifying pharmacological agent for stroke therapy.

C-Phycocyanin ameliorates experimental autoimmune encephalomyelitis and induces regulatory T cells.

For decades Experimental Autoimmune Encephalitis (EAE) has remained as an unsurpassed multiple sclerosis (MS) animal model. C-Phycocyanin (C-Pc) has been reported to exhibit pharmacological properties that may be expected to symptomatically improve EAE and MS. However, in this paper we reveal a basic underlying mechanism that may provide a new approach to the rationale of the overall beneficial effect of this natural antioxidant. We demonstrate that C-Pc is able to trigger mechanisms preventing or downgrading EAE expression and induces a regulatory T cell (Treg) response, in peripheral blood mononuclear cells (PBMC) from MS patients. These results agree with reports suggesting that Treg limit acute MS attacks and that C-Pc may act as a neuroprotector and thereby reverts the organic and functional damage in neurodegenerative disorders of the central nervous system (CNS). Moreover, evidence is provided on the antioxidant activity of C-Pc within the CNS, intended to improve the myelin and axonal damage of EAE induced Lewis rats. Our results indicate that specific Treg activation may represent a central and essential mechanism in supporting the therapeutic potential of C-Pc for MS and may lead to new and more effective therapies; this property would then complement and enhance other proven active principles such as interferons (IFN), giving rise to combined therapies.