Harnessing immunotherapy to combat COVID-19: A modern snake oil or silver bullet?

Coronavirus disease 2019 (COVID-19), an infectious disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2), has emerged into a global health and economic menace. Amidst the COVID-19 turmoil, recent failures/uncertain outcomes in clinical trials involving the anti-malarial (hydroxychloroquine), anti-viral (remdesivir) or the combination of anti-malarial/antibiotic (hydroxychloroquine/azithromycin) regimens have predisposed the physicians to distrust these "highly-touted" drugs for COVID-19. In this milieu, immunotherapy might be a credible modality to target or modify specific/non-specific immune responses that interfere with the survival of intracellular pathogens.

3,4-Dihydroxyphenylethanol Assuages Cognitive Impulsivity in Alzheimer's Disease by Attuning HPA-Axis via Differential Crosstalk of α7 nAChR with MicroRNA-124 and HDAC6.

Cognitive impulsivity, a form of suboptimal cost-benefit decision making, is an illustrious attribute of an array of neurodegenerative diseases including Alzheimer's disease (AD). In this study, a delay discounting paradigm was used to assess the effect of 3,4-dihydroxyphenylethanol (DOPET) on cognitive impulsivity, in an oA42i (oligomeric amyloid β plus ibotenic acid) induced AD mouse model, using a nonspatial T-maze task. The results depicted that oA42i administration elevated cognitive impulsivity, whereas DOPET treatment attenuated the impulsive behavior and matched the choice of the sham-operated controls.

3,4-dihydroxyphenylethanol attenuates spatio-cognitive deficits in an Alzheimer's disease mouse model: modulation of the molecular signals in neuronal survival-apoptotic programs.

Alzheimer's disease (AD), the most common type of dementia, is a devastating neurodegenerative disease characterized by progressive neuro-cognitive dysfunction. In our study, we investigated the potential of 3,4-dihydroxyphenylethanol (DOPET), a dopamine metabolite, and also a polyphenol from olive oil, in ameliorating soluble oligomeric amyloid β1-42 plus ibotenic acid (oA42i)-induced neuro-behavioral dysfunction in C57BL/6 mice. The results depicted that intracerebroventricular injection of oA42i negatively altered the spatial reference and working memories in mice, whereas DOPET treatment significantly augmented the spatio-cognitive abilities against oA42i.

Influence of alpha lipoic acid on antioxidant status in D-galactosamine-induced hepatic injury.

D-Galactosamine (GalN)-induced liver injury is associated with reactive oxygen species and oxidative stress. In the present study, we evaluated the effect of alpha lipoic acid (ALA) supplementation on acute GalN-induced oxidative liver injury. Hepatotoxicity induced by single intraperitoneal injection of GalN (500 mg/kg body wt) was evident from increase in lipid peroxidation and serum marker enzymes (asparate transaminase, alanine transaminase, alkaline phosphatase, and lactate dehydrogenase).

Mitigation of azathioprine-induced oxidative hepatic injury by the flavonoid quercetin in wistar rats.

ABSTRACT Azathioprine (AZA), one of the widely prescribed immunosuppressant drugs in organ transplantation and autoimmune diseases, could cause hepatotoxicity in the course of therapy. The current work was designed to assess the protective role of the dietary flavonoid, quercetin (QE), in oxidative hepatic damage induced by AZA. Adult male Wistar rats were divided into four treatment groups.