Oxidative Stress and Antioxidant Markers in Oral Submucous Fibrosis:A Systematic Review and Meta-Analysis of Case-Control Studies DOI Creative Commons
Jincai Guo, Hui Xie,

Xueru Chen

et al.

Journal of Evidence Based Dental Practice, Journal Year: 2024, Volume and Issue: 25(1), P. 102073 - 102073

Published: Nov. 29, 2024

Language: Английский

In Vitro and In Vivo Antioxidant and Immune Stimulation Activity of Wheat Product Extracts DOI Open Access
Beatrice Mengoni, Federica Armeli, Emily Schifano

et al.

Nutrients, Journal Year: 2025, Volume and Issue: 17(2), P. 302 - 302

Published: Jan. 16, 2025

Inflammation and oxidative stress are the main pathogenetic pathways involved in development of several chronic degenerative diseases. Our study is aimed at assessing antioxidant anti-inflammatory activity hydroalcoholic extracts obtained from wheat its derivatives. The content total phenolic flavonoid compounds were carried out by ABTS DPPH assays. ability to promote microglia polarization towards an phenotype was evaluated analyzing increased expression markers real-time qPCR immunofluorescence Antioxidant all C. elegans ROS levels enzymes GST-4 SOD-3 fluorescence experiments. key genes innate immune response resistance pathways-daf-16, sek-1, pmk-1-was qPCR. Wheat showed polarize cells phenotype, even after addition LPS. An detected both Caenorhabditis nematode, where also implemented anti-stress resilience stimulated immunity. present shows that seeds, flour, chaff, pasta as well activities may be considered prospective positive health agents for preparation functional foods. Moreover, valorization by-products agricultural agro-industrial would have significant implications terms circular economy.

Language: Английский

Citations

3

Neuroinflammaging and the Immune Landscape: The Role of Autophagy and Senescence in Aging Brain DOI Creative Commons

Rajesh Tamatta,

Varsha Pai,

Charu Jaiswal

et al.

Biogerontology, Journal Year: 2025, Volume and Issue: 26(2)

Published: Feb. 5, 2025

Abstract Neuroinflammation is closely linked to aging, which damages the structure and function of brain. It caused by intricate interactions immune cells in aged brain, such as dysregulated glial dysfunctional astrocytes. Aging-associated chronic low inflammation, referred neuroinflammaging, shows an upregulated proinflammatory response. Autophagy senescence play crucial roles moderators aging neuroinflammatory responses. The neuroimmune system, dystrophic cells, release factors alter blood-brain barrier, causing a landscape. Chronic inflammation combined with deteriorating neurons exacerbate neurological disorders decline cognitive function. This review highlights neuroinflammaging mechanism associated interplay central nervous system cellular senescence, autophagy regulation brain's under conditions. Moreover, microglia peripheral process brain have also been discussed. Determining treatment targets comprehending mechanisms that influence necessary decrease neuroinflammation.

Language: Английский

Citations

1

SQSTM1/p62 from Litopenaeus vannamei is involved in the immune response to Vibrio infection DOI

Junliang Luo,

Wei Lu, Yanghui Chen

et al.

Fish & Shellfish Immunology, Journal Year: 2025, Volume and Issue: unknown, P. 110161 - 110161

Published: Jan. 1, 2025

Language: Английский

Citations

0

Multiple Neuropathologies Underly Hippocampal Subfield Atrophy in a Case With a Slowly Progressive Amnestic Syndrome: Challenging the Notion of Pure LATENC DOI Open Access
Hossam Youssef, Rodolfo G. Gatto,

Nha Trang Thu Pham

et al.

Neuropathology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 20, 2025

ABSTRACT Alzheimer's disease (AD) is the leading cause of dementia in elderly, marked by abnormal protein buildup (beta‐amyloid and tau) resulting neuronal loss, especially medial temporal lobe other limbic regions. The presence transactive response DNA binding 43 (TDP‐43) immunoreactive inclusions regions has also been associated with neuroimaging changes It proposed that hypometabolism on [ 18 F] fluorodeoxyglucose positron emission tomography (FDG‐PET) a patient slowly evolving amnestic syndrome may be signature TDP‐43. In this context, we observed an 86‐year‐old Caucasian female characterized syndrome, along focal atrophy evident MRI FDG‐PET. subsequently died underwent autopsy. We performed detailed digital neuropathological analyses hippocampal subfields to better understand relationship between clinico‐imaging findings histopathology. addition TDP‐43, identified three pathological processes lobe: sequestosome‐1/p62, argyrophilic grain (AGD), primary age‐related tauopathy (PART). Hippocampal subfield volumes rates were no different from those matched healthy controls, except for rate cornu ammonis 1 (CA1). Digital histopathology revealed relative highest burden pathology p62, followed AGD, PART CA1. Multiple appear have contributed our progressive syndrome.

Language: Английский

Citations

0

Melatonin augments anti-tumor activity and alleviates nephrotoxicity of gemcitabine in a pancreatic cancer xenograft model targeting P62/Keap1 pathway DOI Creative Commons
Samar Ibrahim,

Eman H. Yousef,

Ahmed M. El‐Dessouki

et al.

Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown

Published: March 18, 2025

Abstract Although gemcitabine is a primary chemotherapy for pancreatic cancer, its effectiveness limited by chemoresistance and nephrotoxicity, posing significant clinical challenges. Therefore, the development of novel therapeutic approaches to prevent malignancy remains crucial. This study aimed investigate potential melatonin in enhancing gemcitabine’s anticancer efficacy while mitigating nephrotoxic effects through modulation Keap1/p62 pathway. A cancer xenograft model was established rats, which received either (50 mg/kg, I.P.), or their combination three times per week 2 weeks. Our findings demonstrate that potentiates cancer-suppressing via Kelch-like-ECH associated protein-1 (Keap1)/p62 pathway, resulting reduced fibrosis, oxidative stress, inflammatory markers. Additionally, significantly mitigated gemcitabine-induced nephrotoxicity. These results suggest may serve as an adjuvant therapy treatment, reducing adverse effects.

Language: Английский

Citations

0

The Probiotic Yeast, Milmed, Promotes Autophagy and Antioxidant Pathways in BV-2 Microglia Cells and C. elegans DOI Creative Commons
Federica Armeli, Beatrice Mengoni, Emily Schifano

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(4), P. 393 - 393

Published: March 27, 2025

Background: Autophagy, a catabolic process essential for maintaining cellular homeostasis, declines with age and unhealthy lifestyles, contributing to neurodegenerative diseases. Probiotics, including Milmed yeast, have demonstrated anti-inflammatory antioxidant properties. This study evaluated the activity of on BV-2 microglial cells in vitro vivo model Caenorhabditis elegans (C. elegans) restoring autophagic processes. Methods: were incubated S. cerevisiae (Milmed treated yeast or untreated yeast) then stimulated lipopolysaccharide (LPS). mRNAs factors enzymes assessed by qPCR; mTOR NRF2 ELISA. pNRF2 compared cytosolic was immunofluorescence. The longevity, body size, reactive oxygen species (ROS) levels C. measured fluorescence microscopy. Results: Treatment YPD cultured dried powder obtained from it promoted flux, as shown increased expression Beclin-1, ATG7, LC3, p62 inhibition mTOR, It also enhanced response increasing NRF2, SOD1, GPX; moreover, enhanced, dietary supplementation prolonged survival reduced age-related ROS accumulation without changing gst-4. pro-longevity effect found be dependent SKN-1/Nrf2 activation, absence benefit skn-1 mutants. Conclusions: demonstrates significant pro-autophagy effects elegans, thereby extending lifespan improving stress resistance, which, together previously activity, highlights its role highly effective probiotic beneficial health effects. Activation SKN-1/NRF2 pathway modulation autophagy support therapeutic potential neuroprotection healthy aging.

Language: Английский

Citations

0

Chronic inflammation in obesity and neurodegenerative diseases: exploring the link in disease onset and progression DOI
Yogita Dhurandhar, Shubham Tomar, Ashmita Das

et al.

Molecular Biology Reports, Journal Year: 2025, Volume and Issue: 52(1)

Published: April 25, 2025

Language: Английский

Citations

0

Curcumin Modulation of the Gut–Brain Axis for Neuroinflammation and Metabolic Disorders Prevention and Treatment DOI Open Access

Michael A. Cerullo,

Federica Armeli, Beatrice Mengoni

et al.

Nutrients, Journal Year: 2025, Volume and Issue: 17(9), P. 1430 - 1430

Published: April 24, 2025

Curcumin, a polyphenolic compound derived from Curcuma longa, has gained significant attention for its potential therapeutic benefits, particularly counteracting inflammation, oxidative stress, and metabolic disorders. Its chemical structure, featuring conjugated double bonds between two aromatic rings, allows it to act as an electron donor, thereby mitigating free radical formation. Despite poor solubility in water, curcumin is stable acidic environments undergoes metabolism both the liver gut. Intestinal microbiota, at colon level, further metabolizes into several derivatives, including dihydrocurcumin tetrahydrocurcumin, which exhibit antioxidant anti-inflammatory properties. Studies suggest that can reduce body mass index (BMI) improve other composition parameters, especially when used combination with lifestyle changes, though bioavailability low due rapid resulting blood concentration. In obesity, dysfunctional adipose tissue remodeling chronic inflammation play critical roles development of complications. Curcumin’s properties are related inhibition NF-κB pathway, leading reduction inflammatory markers adipocytes macrophages. Additionally, modulates stress by activating NRF2 enhancing cellular defenses. Emerging evidence also supports curcumin’s improving gut health modulating microbiota composition, intestinal barrier function, reducing systemic inflammation. This interaction gut–brain axis highlights broader implications neuroprotection, positively affects cognitive function mitigates neuroinflammation neurodegenerative diseases like Alzheimer’s. disease. Thus, holds promise multifaceted agent management obesity associated diseases.

Language: Английский

Citations

0

Erinacine A-Enriched Hericium erinaceus Mycelium Ethanol Extract Lessens Cellular Damage in Cell and Drosophila Models of Spinocerebellar Ataxia Type 3 by Improvement of Nrf2 Activation DOI Creative Commons
Yu‐Ling Wu,

Hai-Lun Sun,

Jui‐Chih Chang

et al.

Antioxidants, Journal Year: 2024, Volume and Issue: 13(12), P. 1495 - 1495

Published: Dec. 7, 2024

Spinocerebellar ataxia type 3 (SCA3), caused by the abnormal expansion of polyglutamine (polyQ) in ataxin-3 protein, is one inherited polyQ neurodegenerative diseases that share similar genetic and molecular features. Mutant polyQ-expanded protein prone to aggregation affected neurons predominantly degraded autophagy, which beneficial for disease treatment. Not only does mutant increase susceptibility oxidative cytotoxicity, but it also hampers antioxidant potency neuronal cells. Nuclear factor erythroid-derived 2-like 2 (Nrf2), a master transcription controls detoxification gene expression, plays crucial role neuroprotection SCA3 other diseases. The present data showed treatment with erinacine A-enriched Hericium erinaceus mycelium ethanol extract (HEME) extended longevity improved locomotor activity ELAV-SCA3tr-Q78 transgenic Drosophila. Moreover, HEME enhanced which, turn, corrected levels restrained both cell Drosophila models SCA3. Markedly, increased activation Nrf2. Silencing Nrf2 expression negated most promising effects on SK-N-SH-MJD78 cells, highlighting critical efficacy These findings suggest has therapeutic potential enhancing autophagic Nrf2-mediated pathways, may influence progression

Language: Английский

Citations

2

Oxidative Stress in the Pathogenesis of Neurodegenerative Diseases DOI Creative Commons
Maria Carolina Jurcău, Anamaria Jurcău,

Radu Diaconu

et al.

Stresses, Journal Year: 2024, Volume and Issue: 4(4), P. 827 - 849

Published: Dec. 2, 2024

Neurodegenerative diseases are devastating conditions with a rising incidence and prevalence due to the aging of population for which we currently do not have efficient therapies. Despite compelling evidence provided by basic research on involvement oxidative stress in their pathogenesis, most trials antioxidants failed. The reasons may relate low bioavailability used compounds or starting therapy late, when pathogenic cascades already induced irreversible damage. current review discusses sources central nervous system, reactive oxygen species pathogenesis Alzheimer’s disease, Parkinson’s amyotrophic lateral sclerosis, importance further improved delivery methods as well search biomarkers that could help early diagnosis hope finding more therapies these diseases.

Language: Английский

Citations

1