Post-traumatic stress disorder and metabolic syndrome: the role of some antioxidants in treatment DOI Creative Commons
Victoria Serhiyenko, A.Yu. Oliinyk, Yaroslav Pavlovskyi

et al.

INTERNATIONAL JOURNAL OF ENDOCRINOLOGY (Ukraine), Journal Year: 2024, Volume and Issue: 20(6), P. 470 - 480

Published: Nov. 9, 2024

The basis for the pathogenesis of cardiovascular, cancer, metabolic diseases, low-grade chronic inflammation (LGCI) and many other disorders is an imbalance between prooxidants antioxidant defense system. It believed that link post-traumatic stress disorder (PTSD) syndrome (MetS) based on oxidative (OS), increased autonomic nervous system activity, glucocorticoid synthesis activation, or immunological dysregulation. Moreover, pathophysiological changes in systemic LGCI pathways result from modifications receptor reactivity (secondary to emotional physiological arousal) may be inappropriate social behavior consistent with PTSD MetS manifestations. Recently, evidence has emerged suggesting a combination high levels OS activation plays important role PTSD. On hand, type recurrent long-term trauma exacerbates accele­rates cellular aging. accompanied by release reactive oxygen nitrogen species, proinflammatory cytokines, biologically active substances cause OS. purpose this review was discuss individual antioxidants, particular polyphenols, flavonoids, carotenoids, N-acetylcysteine, melatonin, L-arginine, C E vitamins, zinc, copper, selenium, prevention/treatment comorbid pathology MetS, as well analyze new trends directions future research. search conducted Scopus, Science Direct (from Else­vier) PubMed, including MEDLINE databases. keywords used were “post-traumatic disorder,” “metabolic syndrome,” “antioxidants.” To identify research results could not found during online search, manual bibliography publications used.

Language: Английский

Kaempferol: Paving the path for advanced treatments in aging-related diseases DOI Creative Commons
Md Sadique Hussain, Abdulmalik Saleh Alfawaz Altamimi, Muhammad Afzal

et al.

Experimental Gerontology, Journal Year: 2024, Volume and Issue: 188, P. 112389 - 112389

Published: March 8, 2024

Aging-related diseases (ARDs) are a major global health concern, and the development of effective therapies is urgently needed. Kaempferol, flavonoid found in several plants, has emerged as promising candidate for ameliorating ARDs. This comprehensive review examines Kaempferol's chemical properties, safety profile, pharmacokinetics, highlights its potential therapeutic utility against underpinned by distinctive structure, which confers antioxidative anti-inflammatory properties. Kaempferol counteracts reactive oxygen species (ROS) modulates crucial cellular pathways, thereby combating oxidative stress inflammation, hallmarks low toxicity wide margins, demonstrated preclinical clinical studies, further substantiate potential. Compelling evidence supports substantial addressing ARDs through mechanisms, notably anti-inflammatory, antioxidant, anti-apoptotic actions. exhibits versatile neuroprotective effect modulating various proinflammatory signaling including NF-kB, p38MAPK, AKT, β-catenin cascade. Additionally, it hinders formation aggregation beta-amyloid protein regulates brain-derived neurotrophic factors. In terms anticancer potential, kaempferol acts diverse inducing apoptosis, arresting cell cycle at G2/M phase, suppressing epithelial-mesenchymal transition (EMT)-related markers, affecting phosphoinositide 3-kinase/protein kinase B pathways. Subsequent studies should focus on refining dosage regimens, exploring innovative delivery systems, conducting trials to translate these findings into applications.

Language: Английский

Citations

48
Therapeutic potential and underlying mechanisms of phytoconstituents: emphasizing on resveratol, curcumin, quercetin, berberine, and hesperidin in ulcerative colitis DOI

Tanuj Gangwar,

Neelam Poonia,

Rudra Narayan Subudhi

et al.

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

Published: Jan. 29, 2025

Language: Английский

Citations

3
Quercetin in the Prevention of Induced Periodontal Disease in Animal Models: A Systematic Review and Meta-Analysis DOI Open Access
Markus Laky, Muazzez Arslan,

Xilei Zhu

et al.

Nutrients, Journal Year: 2024, Volume and Issue: 16(5), P. 735 - 735

Published: March 4, 2024

Background: Periodontitis is an inflammatory condition initiated by oral bacteria and associated with several systemic diseases. Quercetin anti-inflammatory anti-bacterial poly-phenol present in various foods. The aim of this meta-analysis was the evaluation effects quercetin administration animal models experimental periodontitis. Methods: A systematic search performed electronic databases using following terms: “periodontitis” or “periodontal disease” “gingivitis” “quercetin” “cyanidanol” “sophoretin” “pentahydroxyflavone”. In vivo preclinical periodontal disease a measurement alveolar bone loss were included analysis. risk bias studies assessed SYRCLE tool. Results: yielded 335 results. Five included, four them qualified for meta-analysis. showed that decreased (τ2 = 0.31, 1.88 mm 95%CI: 1.09, 2.67) models. However, assessment indicated domains had high bias. Conclusions: diminishes prevents progression disease. might facilitate tissue hemostasis reducing senescent cells, decreasing oxidative stress via SIRT1-induced autophagy, limiting inflammation, fostering bacterial microenvironment symbiotic microbiota health. Future research will show whether how promising results can be translated into clinical treatment

Language: Английский

Citations

10
Icariin prevents methylmercury-induced experimental neurotoxicity: Evidence from cerebrospinal fluid, blood plasma, brain samples, and in-silico investigations DOI Creative Commons

Sarthak Sharma,

Sidharth Mehan, Zuber Khan

et al.

Heliyon, Journal Year: 2024, Volume and Issue: 10(1), P. e24050 - e24050

Published: Jan. 1, 2024

Amyotrophic Lateral Sclerosis (ALS) is a fatal neurodegenerative disease that causes significant neurodegeneration. Methylmercury (MeHg) neurotoxin induces axonal neurodegeneration and motor nerve degeneration by destroying oligodendrocytes, degenerating white matter, inducing apoptosis, excitotoxicity, reducing myelin basic protein (MBP). This study examines the inhibition of SIRT-1 (silence information regulator 1), Nrf-2 (nuclear factor E2-related 2), HO-1 (heme oxygenase TDP-43 (TAR-DNA-binding 43) accumulation in context ALS, as well modulation these proteins icariin (15 30 mg/kg, orally), glycoside flavonoid with neuroprotective properties. Neuroprotective activates SIRT-1, Nrf-2, HO-1, mitigating inflammation neuronal injury disorders. In-vivo in-silico testing experimental ALS models confirmed efficacy modulating cellular targets. The addition sirtinol 10 an inhibitor helps determine effectiveness icariin. In this study, we also examined neurobehavioral, neurochemical, histopathological, LFB (Luxol fast blue) markers various biological samples, including Cerebrospinal fluid (CSF), blood plasma, brain homogenates (Cerebral Cortex, Hippocampus, Striatum, mid-brain, Cerebellum). These results demonstrate administration ameliorates mechanism underlying benefits likely related to regulating signaling pathways.

Language: Английский

Citations

9
Curcumin regulates autophagy through SIRT3-SOD2-ROS signaling pathway to improve quadriceps femoris muscle atrophy in KOA rat model DOI Creative Commons

Hua Ye,

Long Yi, Jia‐ming Yang

et al.

Scientific Reports, Journal Year: 2024, Volume and Issue: 14(1)

Published: April 8, 2024

Abstract Knee osteoarthritis (KOA) usually leads to quadriceps femoris atrophy, which in turn can further aggravate the progression of KOA. Curcumin (CUR) has anti-inflammatory and antioxidant effects been shown be a protective agent for skeletal muscle. CUR have effect on However, there are no studies related whether improves KOA-induced muscle atrophy. We established model KOA rats. Rats experimental group were fed 5 weeks. Changes autophagy levels, reactive oxygen species (ROS) changes expression Sirutin3 (SIRT3)-superoxide dismutase 2 (SOD2) pathway detected led was induced ROS levels increased. increased SIRT3 expression, decreased SOD2 acetylation inhibited over-activation autophagy, thereby alleviating atrophy improving against is alleviated after improvement with possible mechanism being reduction ROS-induced via SIRT3-SOD2 pathway.

Language: Английский

Citations

9
SIRT3: A potential therapeutic target for liver fibrosis DOI
Yan Ning,

Xinyue Dou,

Zhichao Wang

et al.

Pharmacology & Therapeutics, Journal Year: 2024, Volume and Issue: 257, P. 108639 - 108639

Published: March 30, 2024

Language: Английский

Citations

8
Targeting sirtuins for cancer therapy: epigenetics modifications and beyond DOI Creative Commons
Hui Shen,

Xinyi Qi,

Yue Hu

et al.

Theranostics, Journal Year: 2024, Volume and Issue: 14(17), P. 6726 - 6767

Published: Jan. 1, 2024

Sirtuins (SIRTs) are well-known as nicotinic adenine dinucleotide

Language: Английский

Citations

8
Resveratrol-driven macrophage polarization: unveiling mechanisms and therapeutic potential DOI Creative Commons
P. L. Wang,

Zhenhong Li,

Yixuan Song

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 13, 2025

Resveratrol, a polyphenolic compound known for its diverse biological activities, has demonstrated multiple pharmacological effects, including anti-inflammatory, anti-aging, anti-diabetic, anti-cancer, and cardiovascular protective properties. Recent studies suggest that these effects are partly mediated through the regulation of macrophage polarization, wherein macrophages differentiate into pro-inflammatory M1 or anti-inflammatory M2 phenotypes. Our review highlights how resveratrol modulates polarization various signaling pathways to achieve therapeutic effects. For example, can activate senescence-associated secretory phenotype (SASP) pathway inhibit signal transducer activator transcription (STAT3) sphingosine-1-phosphate (S1P)-YAP axes, promoting suppressing thereby inhibiting tumor growth. Conversely, it promote suppress by NF-κB activating PI3K/Akt AMP-activated protein kinase (AMPK) pathways, thus alleviating inflammatory responses. Notably, effect on is concentration-dependent; moderate concentrations tend while higher may favor polarization. This concentration dependence offers new perspectives clinical treatment but also underscores necessity precise dosage control when using resveratrol. In summary, exhibits significant potential in regulating treating related diseases.

Language: Английский

Citations

1
Factors influencing glycocalyx degradation: a narrative review DOI Creative Commons
Jing Wang, Lan Ma, Fang Yu

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 16, 2025

The glycocalyx is a layer of villus-like structure covering the luminal surface vascular endothelial cells. Damage to has been proven linked development many diseases. However, factors that promote damage are not fully elaborated. This review summarizes leading reduction in detail, including inflammatory factors, ischemia-reperfusion, oxidative stress, lipids, glucose, high sodium, female sex hormones and others. Additionally, mechanisms underlying its degradation discussed. To better prevent treat related diseases induced by degradation, it meaningful measure avoid these factors.

Language: Английский

Citations

1
Resveratrol-Enhanced Human Neural Stem Cell-Derived Exosomes Mitigate MPP+-Induced Neurotoxicity Through Activation of AMPK and Nrf2 Pathways and Inhibition of the NLRP3 Inflammasome in SH-SY5Y Cells DOI Creative Commons
Tony F. Chan, Yuping Yang, Christopher J.B. Nicol

et al.

Life, Journal Year: 2025, Volume and Issue: 15(2), P. 294 - 294

Published: Feb. 13, 2025

Parkinson's disease (PD) is a progressive neurodegenerative disorder primarily characterized by the loss of dopaminergic neurons in substantia nigra. Mitochondrial dysfunction, oxidative stress, and neuroinflammation are recognized as critical pathological mechanisms driving neurodegeneration PD. Exosome (Exo)-based therapies, particularly those derived from human neural stem cells (hNSCs), offer promising neuroprotective effects due to their ability transfer bioactive molecules that modulate cellular processes. Resveratrol (RES), polyphenolic compound with potent antioxidant anti-inflammatory properties, has been shown enhance therapeutic potential cell (SC)-derived Exos. This study investigated RES-treated hNSCs-derived Exos (RES-hNSCs-Exos) on SH-SY5Y exposed 1-methyl-4-phenylpyridinium (MPP+), neurotoxin commonly used model Parkinsonian neurotoxicity. Treating MPP+ led significant reductions viability, mitochondrial increased activation inflammatory pathways. Treatment RES-hNSCs-Exos rescued MPP+-induced toxicity improving enhancing ATP production, increasing biogenesis, reducing reactive oxygen species (ROS) generation. The findings also demonstrated expression essential genes involved such PGC1α, NRF1, Tfam, indicating improved function presence RES-hNSCs-Exos. Further analysis revealed these protective were mediated activating AMP-activated protein kinase (AMPK) Nrf2 signaling pathways, which promoted health reduced stress. Moreover, treatment suppressed downregulating NLRP3 inflammasome secretion pro-inflammatory cytokines IL-1β IL-18. In conclusion, results suggest exhibit against neurotoxicity function, inhibiting neuroinflammation. These highlight hNSCs-Exos novel strategy for diseases like PD, RES valuable enhancer efficacy.

Language: Английский

Citations

1