Molecular Neurobiology, Год журнала: 2025, Номер unknown
Опубликована: Апрель 9, 2025
Язык: Английский
Scientific Reports, Год журнала: 2024, Номер 14(1)
Опубликована: Май 10, 2024
COVID-19, caused by SARS-CoV-2, affects neuronal cells, causing several symptoms such as memory loss, anosmia and brain inflammation. Curcuminoids (Me08 e Me23) curcumin (CUR) are derived from Curcuma Longa extract (EXT). Many therapeutic actions have been linked to these compounds, including antiviral action. Given the severe implications of especially within central nervous system, our study aims shed light on potential curcuminoids against SARS-CoV-2 infection, particularly in cells. Here, we investigated effects CUR, EXT, Me08 Me23 human neuroblastoma SH-SY5Y. We observed that significantly decreased expression plasma membrane-associated transmembrane protease serine 2 (TMPRSS2) TMPRSS11D, consequently mitigating elevated ROS levels induced SARS-CoV-2. Furthermore, exhibited antioxidative properties increasing NRF2 gene restoring NQO1 activity following infection. Both effectively reduced replication SH-SY5Y cells overexpressing ACE2 (SH-ACE2). Additionally, all compounds demonstrated ability decrease proinflammatory cytokines IL-6, TNF-α, IL-17, while specifically INF-γ levels. Our findings suggest curcuminoid could serve a agent for impact context system involvement.
Язык: Английский
Процитировано
18
Biomedicines, Год журнала: 2025, Номер 13(2), С. 485 - 485
Опубликована: Фев. 16, 2025
The intersection of COVID-19 and cardiovascular disease (CVD) has emerged as a significant area research, particularly in understanding the impact antiplatelet therapies like ticagrelor clopidogrel. been associated with acute complications, including myocardial infarction, thrombosis, heart failure, exacerbated by virus's ability to trigger widespread inflammation endothelial dysfunction. MicroRNAs (miRNAs) play critical role regulating these processes modulating gene expressions involved platelet function, inflammation, vascular homeostasis. This study explores potential miRNAs such miR-223 miR-126 biomarkers for predicting resistance or responsiveness patients disease. Identifying miRNA signatures linked drug efficacy could optimize treatment strategies at high risk thrombotic events during infection. Moreover, miRNA-mediated pathways offers new insights into how SARS-CoV-2 exacerbates CVD, through mechanisms cytokine storms damage. findings this research lead personalized therapeutic approaches, improving patient outcomes reducing mortality COVID-19-associated events. With global implications, addresses urgent need effective management CVD context COVID-19, focusing on integration molecular enhance precision therapy.
Язык: Английский
Процитировано
2
Life, Год журнала: 2025, Номер 15(1), С. 113 - 113
Опубликована: Янв. 16, 2025
The COVID-19 pandemic caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has profoundly impacted global health, with pneumonia emerging as a major complication in severe cases. pathogenesis of is marked the overproduction reactive oxygen species (ROS) and an excessive inflammatory response, resulting oxidative stress significant tissue damage, particularly respiratory system. Antioxidants have garnered considerable attention for their potential role managing mitigating modulating immune responses. This review provides comprehensive overview literature on use antioxidants hospitalized patients mild-to-moderate COVID-19. Studies exploring antioxidants, including vitamins, trace elements, nitric oxide (NO), ozone (O3), glutathione (GSH), L-carnitine, melatonin, bromelain, N-acetylcysteine (NAC), numerous polyphenols, yielded promising outcomes. Through ROS-scavenging properties, these molecules support endothelial function, reduce thrombosis risk, may help mitigate effects cytokine storm, key contributor to morbidity mortality. Clinical evidence suggests that antioxidant supplementation improve patient outcomes decreasing inflammation, supporting cell potentially shortening recovery times. Furthermore, symptoms exerting direct antiviral inhibit infection process genomic replication SARS-CoV-2 host cells. Moreover, work synergistically standard treatments viral-induced damage. By integrating findings from real-world data our clinical experience, we gain more profound understanding pneumonia. Further research combining reviews analysis crucial validate efficacy establish evidence-based guidelines practice.
Язык: Английский
Процитировано
1
Pharmacology & Therapeutics, Год журнала: 2024, Номер 260, С. 108684 - 108684
Опубликована: Июль 2, 2024
Язык: Английский
Процитировано
7
American Journal of Human Biology, Год журнала: 2025, Номер 37(1)
Опубликована: Янв. 1, 2025
ABSTRACT Oxidative stress (OS) is a key biological challenge and selective pressure for organisms with aerobic metabolism. The result of the imbalance between reactive oxygen species production antioxidant defense, OS can damage proteins, lipids, nucleic acids plays an important role in driving variation aging health. Among humans, research has focused overwhelmingly on adults, demonstrated connections OS, inflammation, metabolic neurodegenerative conditions. Relatively little attention been given to during childhood adolescence. This lack early life exists despite clear implications informing human history evolution, subadult development, lifelong Here, we review current knowledge subadulthood. Our objectives are threefold: (1) To highlight common methods measuring among children adolescents establish typical measurement values; (2) summarize evidence linking demographic ecological factors OS; (3) identify avenues future biology. underscores expanding methodological toolkit assessing adolescents. Subadult considerably elevated compared pattern eliciting unknown consequences likely related increased demands (e.g., unique brain development). Factors such as diet, physical activity, infectious disease, structural neglect also appear drive OS. Current limitations evident. Future work should emphasize evolutionary, biocultural, energetic course perspectives advance this promising area
Язык: Английский
Процитировано
1
Biology, Год журнала: 2023, Номер 12(8), С. 1070 - 1070
Опубликована: Июль 30, 2023
Signs and symptoms involving multiple organ systems which persist for weeks or months to years after the initial SARS-CoV-2 infection (also known as PASC long COVID) are common complications of individuals with COVID-19. We recently reported pathophysiological changes in various organs post-acute mice mouse hepatitis virus-1 (MHV-1, a coronavirus) (7 days) long-term post-infection (12 months). One severely affected this animal model is kidney, correlated well human studies showing kidney injury post-SARS-CoV-2 infection. Our pathological observation kidneys includes development edema inflammation renal parenchyma, severe acute tubular necrosis, infiltration macrophages lymphocytes, addition observed both post-infection, include epithelial cell degenerative changes, peritubular vessel congestion, proximal distal hemorrhage interstitial tissue, vacuolation tubules. These findings strongly suggest possible fibrosis, particular post-infection. Accordingly, we investigated whether signaling system that initiate above-mentioned other conditions also activated post-MHV-1 found increased TGF-β1, FGF23, NGAL, IL-18, HIF1-α, TLR2, YKL-40, B2M mRNA levels infection, but not EGFR, TNFR1, BCL3, WFDC2. However, only neutrophil gelatinase-associated lipocalin (NGAL) days). Immunoblot showed an elevation protein TLR-2, EGFR while KIM-1 MMP-7 Treatment synthetic peptide, SPIKENET (SPK), inhibits spike binding, reduced NGAL decreased BCL3 mRNA, TLR-2 fibrotic events may early leading pronounced fibrosis COVID. Targeting these factors therapeutically prevent long-COVID-associated complications.
Язык: Английский
Процитировано
16
Frontiers in Immunology, Год журнала: 2023, Номер 14
Опубликована: Авг. 15, 2023
COVID-19 is characterized by an excessive inflammatory response and macrophage hyperactivation, leading, in severe cases, to alveolar epithelial injury acute respiratory distress syndrome. Recent studies have reported that SARS-CoV-2 spike (S) protein interacts with bacterial lipopolysaccharide (LPS) boost responses vitro, macrophages peripheral blood mononuclear cells (PBMCs), vivo. The hypothalamic hormone growth hormone-releasing (GHRH), addition promoting pituitary GH release, exerts many functions, acting as a factor both malignant non-malignant cells. GHRH antagonists, turn, display potent antitumor effects antinflammatory activities different cell types, including lung endothelial However, date, the role of antagonists remains unexplored. Here, we examined ability antagonist MIA-602 reduce inflammation human THP-1-derived PBMCs stimulated S LPS combination. Western blot immunofluorescence analysis revealed presence receptor its splice variant SV1 THP-1 PBMCs. Exposure combination increased mRNA levels secretion TNF-α IL-1β, well IL-8 MCP-1 gene expression, effect hampered MIA-602. Similarly, hindered IL-1β reduced levels. Mechanistically, blunted LPS-induced activation pathways cells, such NF-κB, STAT3, MAPK ERK1/2 JNK. also attenuated oxidative stress PBMCs, decreasing ROS production, iNOS COX-2 levels, MMP9 activity. Finally, prevented synergism on NF-кB nuclear translocation Overall, these findings demonstrate novel for MIA class suggest their potential development treatment diseases, related comorbidities.
Язык: Английский
Процитировано
13
Life, Год журнала: 2024, Номер 14(4), С. 460 - 460
Опубликована: Апрель 1, 2024
In severe cases, SARS-CoV-2 infection leads to respiratory failure. Although angiotensin-converting enzyme 2 (ACE2) receptors are not expressed in red blood cells, can interact with cells (RBCs) via several or auxiliary membrane proteins. Recent data show that viral causes significant damage the RBCs, altering their morphology, deformability, and aggregability. Loss of RBC deformability and/or increased aggregability favors development thrombotic processes microcirculation, as has been described occur COVID-19 patients. addition, many patients also develop systemic endotheliitis associated generalized coagulopathy. This manifests itself clinically obstructive microthrombi area medium smallest vessels, which affect all internal organs. It is thought such changes RBCs may contribute microangiopathy/microthrombosis result impaired capillary flow tissue oxygenation.
Язык: Английский
Процитировано
5
International Journal of Molecular Sciences, Год журнала: 2024, Номер 25(7), С. 3805 - 3805
Опубликована: Март 29, 2024
The post-COVID condition (PCC) is a pathology stemming from COVID-19, and studying its pathophysiology, diagnosis, treatment crucial. Neuroinflammation causes the most common manifestations of this disease including headaches, fatigue, insomnia, depression, anxiety, among others. Currently, there are no specific management proposals; however, given that inflammatory component involves cytokines free radicals, these conditions must be treated to reduce current symptoms provide neuroprotection risk long-term neurodegenerative disease. It has been shown cannabis compounds with immunomodulatory antioxidant functions in other pathologies. Therefore, exploring approach could viable therapeutic option for PCC, which purpose review. This review involved an exhaustive search specialized databases PubMed, PubChem, ProQuest, EBSCO, Scopus, Science Direct, Web Science, Clinical Trials. Phytocannabinoids, cannabidiol (CBD), cannabigerol (CBG), Delta-9-tetrahydrocannabinol (THC), exhibit significant antioxidative anti-inflammatory properties have effective neuroinflammatory conditions. These promising adjuvants PCC alone or combination antioxidants therapies. presents challenges neurological health, neuroinflammation oxidative stress play central roles pathogenesis. Antioxidant therapy cannabinoid-based approaches represent areas research mitigating adverse effects, but further studies needed.
Язык: Английский
Процитировано
5
Journal of General Virology, Год журнала: 2023, Номер 104(11)
Опубликована: Ноя. 10, 2023
The recent coronavirus disease 2019 (COVID-19) pandemic was caused by severe acute respiratory syndrome 2 (SARS-CoV-2). COVID-19 is characterized distress, multiorgan dysfunction and, in some cases, death. virus also responsible for post-COVID-19 condition (commonly referred to as ‘long COVID’). SARS-CoV-2 a single-stranded, positive-sense RNA with genome of approximately 30 kb, which encodes 26 proteins. It has been reported affect multiple pathways infected cells, resulting, many the induction ‘cytokine storm’ and cellular senescence. Perhaps because it an virus, replicating largely cytoplasm, effect SARS-Cov-2 on stability DNA damage responses (DDRs) received relatively little attention. However, now becoming clear that causes DNA, shown presence micronuclei, repair foci increased comet tails cells. This review considers evidence indicating how instability, deregulates cell cycle targets specific components DDR pathways. significance virus’s ability cause senescence considered, are implications instability patients suffering from long COVID.
Язык: Английский
Процитировано
11