ABSTRACT
This study aimed to assess the association between serum zinc level with some inflammatory and immunity factors and the duration of hospitalization and mortality rate in patients diagnosed with Covid-19. In this cross-sectional study, blood samples were taken from polymerase chain reaction (PCR) positive patients. New patients diagnosed with Covid-19, admitted to different public hospital wards, were considered eligible for entering the study. The study was done on 179 hospitalized patients diagnosed with Covid-19. Fourteen patients died during the hospitalization and the in-hospital mortality rate was 7.8%, with 9.1% (13 patients) of patients with serum zinc level less than 70 mcg/dL and 3.4% (1 patient) of patients with zinc levels more than 70 mcg/dL. Higher levels of zinc were significantly associated with a higher and lower level of interferon-gamma (IFN-γ) (p-value = 0.035) and interleukin (IL)-6 (p-value = 0.004), respectively. The level of serum zinc did not have a significant association with mortality even after adjusting for confounding factors. The relationship between zinc level and the duration of hospitalization was also not significant. In conclusion, serum zinc level had an association with IL-6 and IFN-γ level, but it did not have any significant association with hospital duration or mortality.
ABSTRACT
Glycogen synthase kinase-3 (GSK-3) is a critical molecule in Alzheimer's disease (AD) that modulates two histopathological hallmarks of AD: Amyloid beta (Aß) plaques and neurofibrillary tangles composed of aberrant hyper-phosphorylation of tau protein. This study was performed to investigate the protective effect of flavone apigenin through inhibition of GSK-3 and the involvement of this kinase in the inhibition of BACE1 expression and hyperphosphorylation of tau protein in an AD rat model. 15 nM of aggregated amyloid-beta 25-35 was microinjected into the left lateral ventricle of an AD rat. Apigenin (50 mg/kg) was administered orally 45 min before the Aß injection and continued daily for three weeks. Immunohistochemistry and western blot analysis showed that apigenin significantly reduced the hyperphosphorylation of tau levels in the hippocampus. Real-time PCR analysis revealed significant inhibition of the mRNA level of ß secretase (BACE1) and GSK-3ß, but Apigenin had no effect on the level of GSK-3α. The results demonstrate that apigenin has a protective effect against amyloid-beta 25-35 by decreasing the expression of GSK-3ß with the consequence of lowering the hyperphosphorylation of tau protein and suppressing BACE1 expression.
Subject(s)
Alzheimer Disease/genetics , Alzheimer Disease/prevention & control , Amyloid beta-Peptides/antagonists & inhibitors , Amyloid beta-Peptides/toxicity , Apigenin/pharmacology , Glycogen Synthase Kinase 3 beta/drug effects , Neuroprotective Agents/pharmacology , Peptide Fragments/antagonists & inhibitors , Peptide Fragments/toxicity , Amyloid Precursor Protein Secretases/biosynthesis , Amyloid Precursor Protein Secretases/genetics , Animals , Aspartic Acid Endopeptidases/biosynthesis , Aspartic Acid Endopeptidases/genetics , Immunohistochemistry , Male , Phosphorylation , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Rats , Rats, Wistar , tau Proteins/metabolismABSTRACT
INTRODUCTION: Cognitive dysfunction is the most common problem of patients with Alzheimer Disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss, synaptic dysfunction, and alteration in neurotransmitters receptors. Mitochondrial synapses dysfunction due to the accumulation of Amyloid Beta (Aß) is one of the earliest pathological features of AD. The flavone apigenin has been reported to play some protective roles in AD through the anti-oxidative and anti-inflammatory properties. This study aimed at investigating the effects of apigenin on spatial working memory and neural protection by restoring mitochondrial dysfunction and inhibition of caspase 9. METHODS: Intracerebroventricular (ICV) microinjection of Aß 25-35 was used for AD modeling. Working memory was assessed 21 days later using the Y maze test. Neuronal loss was detected in the hilar area of the hippocampus using Nissl and Fluoro-jade B staining, whereas immunohistochemistry was used to illustrate cytochrome c positive cells and caspase 9. RESULTS: The results revealed that apigenin significantly ameliorated spatial working memory. It also significantly reduced the number of degenerative neurons in the hilus area. Apigenin almost completely blocked the release of cytochrome c and caspase 9 in hilus. CONCLUSION: Apigenin may improve the spatial working memory deficits and neuronal degeneration through the amelioration of the mitochondrial dysfunction.
