Ameliorative effect of gallic acid on cisplatin-induced ovarian toxicity in rats DOI
Elif Ayazoğlu Demir, Ahmet Menteşe,

Ayten Livaoğlu

et al.

Drug and Chemical Toxicology, Journal Year: 2021, Volume and Issue: 46(1), P. 97 - 103

Published: Dec. 9, 2021

The aim of the present study was to evaluate protective effect gallic acid (GA) against cisplatin (CDDP)-induced ovarian toxicity, for first time. damage generated with CDDP (5 mg/kg) intraperitoneally (i.p.) administration in rats. GA (2.5 and 5 were administered i.p. 3 consecutive days. carried out main groups containing 6 rats each group: control, mg/kg), CDDP, + mg/kg). levels malondialdehyde (MDA), total oxidant status (TOS), antioxidant (TAS), oxidative stress index (OSI), catalase (CAT), 8-hydroxy-2'-deoxyguanosine (8-OHdG), caspase-3 tumor necrosis factor-alpha (TNF-α) determined. Hematoxylin eosin staining method employed histopathological examination. In group, it is determined that statistically significant decreasing TAS CAT, increasing MDA, TOS, OSI, 8-OHdG, TNF-α (p < 0.05) compared control group. administrations significantly restored this 0.05). Although vascular congestion, edema, hemorrhage, follicular degeneration leukocyte infiltration higher group than these damages conclusion, showed prevented CDDP-induced its antioxidant, anti-apoptotic anti-inflammatory activities. More comprehensive studies are needed see underlying mechanisms.

Language: Английский

Biomarkers in Stress Related Diseases/Disorders: Diagnostic, Prognostic, and Therapeutic Values DOI Creative Commons
Kuldeep Dhama,

Shyma K. Latheef,

Maryam Dadar

et al.

Frontiers in Molecular Biosciences, Journal Year: 2019, Volume and Issue: 6

Published: Oct. 18, 2019

Various internal and external factors negatively affect the homeostatic equilibrium of organisms at molecular to whole-body level, inducing so-called state 'stress'. Stress affects an organism's welfare status induces energy-consuming mechanisms combat subsequent ill effects; thus, individual may be immunocompromised, making them vulnerable pathogens. The information presented here has been extensively reviewed, compiled analyzed from authenticated published resources available on Medline, Pubmed, Pubmed Central, Science Direct, other scientific databases. levels can monitored by quantitative qualitative measurement biomarkers. Prominent markers stress include thermal like heat shock proteins (HSPs), innate immune Acute Phase Proteins (APPs), oxidative markers, chemical secretions in saliva urine. In addition, biomarkers are thought play critical roles prognosis stress-related diseases disorders, therapy guidance. Moreover, different components have identified as potent mediators cardiovascular, central nervous system, hepatic, nephrological which also employed evaluate these conditions precisely, but with stringent validation specificity. Considerable advances made detection, quantitation, application present review describes current progress identifying biomarkers, their prognostic therapeutic values.

Language: Английский

Citations

252

Insulin Resistance and Oxidative Stress in the Brain: What’s New? DOI Open Access
Mateusz Maciejczyk, Ewa Żebrowska, Adrian Chabowski

et al.

International Journal of Molecular Sciences, Journal Year: 2019, Volume and Issue: 20(4), P. 874 - 874

Published: Feb. 18, 2019

The latest studies have indicated a strong relationship between systemic insulin resistance (IR) and higher incidence of neurodegeneration, dementia, mild cognitive impairment. Although some these abnormalities could be explained by chronic hyperglycaemia, hyperinsulinemia, dyslipidaemia, and/or prolonged whole-body inflammation, the key role is attributed to neuronal redox imbalance oxidative damage. In this mini review, we provide schematic overview intracellular stress mitochondrial in IR brain. We highlight important correlations found so far brain stress, ceramide generation, β-amyloid accumulation, as well apoptosis conditions.

Language: Английский

Citations

203

Alzheimer’s Disease as Type 3 Diabetes: Common Pathophysiological Mechanisms between Alzheimer’s Disease and Type 2 Diabetes DOI Open Access
Michail Michailidis, Despina Μoraitou, Despina Α. Tata

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(5), P. 2687 - 2687

Published: Feb. 28, 2022

Globally, the incidence of type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD) epidemics is increasing rapidly has huge financial emotional costs. The purpose current review article to discuss shared pathophysiological connections between AD T2DM. Research findings are presented underline vital role that insulin plays in brain’s neurotransmitters, homeostasis energy, as well memory capacity. this indicate existence a mechanistic interplay pathogenesis with T2DM and, especially, disrupted signaling. interlinked resistance, neuroinflammation, oxidative stress, advanced glycosylation end products (AGEs), mitochondrial dysfunction metabolic syndrome. Beta-amyloid, tau protein amylin can accumulate brains. Given patients not routinely evaluated terms their cognitive status, they rarely treated for impairment. Similarly, high levels or Studies suggesting caused by resistance brain also offer strong support hypothesis 3 diabetes.

Language: Английский

Citations

163

The brain as an insulin-sensitive metabolic organ DOI Creative Commons
Joshua L. Milstein, Heather A. Ferris

Molecular Metabolism, Journal Year: 2021, Volume and Issue: 52, P. 101234 - 101234

Published: April 16, 2021

The brain was once thought of as an insulin-insensitive organ. We now know that the insulin receptor is present throughout and serves important functions in whole-body metabolism function. Brain signaling involved not only homeostatic processes but also neuropathological such cognitive decline Alzheimer's disease.

Language: Английский

Citations

147

Obesity: Pathophysiology, monosodium glutamate-induced model and anti-obesity medicinal plants DOI Open Access
René Hernández-Bautista, Ayman M. Mahmoud, Mina Königsberg

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2018, Volume and Issue: 111, P. 503 - 516

Published: Dec. 28, 2018

Obesity and overweight have increased at an alarming rate in the world during last three decades. is a crucial factor development of metabolic abnormalities, including glucose intolerance, insulin resistance, syndrome, low-grade inflammation oxidative stress. A similar scinario occurs aging process where alterations energetic metabolism homeostasis chronic systematic been observed. Oxidative stress poor physical performance can increase risk disease. Despite diverse studies on pathophysiological effects obesity, its impact related to gender through life, particularly aging, hasn’t received reasonable attention. The purpose this review outline mechanisms associated with emphasis monosodium glutamate (MSG)-induced obese model. MSG-induced obesity declined adiponectin were more obvious male mice, while tolerance, sensitivity redox balance altered age both female mice. These findings indicate that are as well aging. Therefore, MSG model resonable value underlie relationship between gender, obesity. In addition, we reviewed medicinal plants their active constituents which used treat Given significat model, needed scrutinize benificial underlying proven anti-obesity activity.

Language: Английский

Citations

124

Neurochemical Modifications in the Hippocampus, Cortex and Hypothalamus of Mice Exposed to Long-Term High-Fat Diet DOI Creative Commons
Blanca Lizarbe, Ana Francisca Soares, Sara Larsson

et al.

Frontiers in Neuroscience, Journal Year: 2019, Volume and Issue: 12

Published: Jan. 8, 2019

Metabolic syndrome and diabetes impact brain function metabolism. While it is well established that rodents exposed to diets rich in saturated fat develop dysfunction, contrasting results abound the literature, likely as result of exposure different high-fat diet (HFD) compositions for varied periods time. In present study, we investigated alterations hippocampal-dependent spatial memory by measuring Y-maze spontaneous alternation, metabolic profiles hippocampus, cortex hypothalamus 1H magnetic resonance spectroscopy (MRS), levels proteins specific synaptic glial compartments mice 6 months amounts (10, 45, or 60% total energy intake). Increasing dietary amount from 10 45% resulted obesity accompanied increased leptin, fasting blood glucose insulin, reduced tolerance. comparison controls (10%-fat), only fed 60%-fat showed glycemia, plasma corticosterone has a major on function. HFD-induced profile modifications measured MRS were observed across three areas 60%- but not 45%-fat diet, while both HFD groups displayed impaired memory. also affected systems involved neuro- gliotransmission hippocampus. Namely, relative controls, 60%-fat-fed SNAP-25, PSD-95 syntaxin-4 immunoreactivity, 45%-fat-fed gephyrin immunoreactivity. For levels, reductions vesicular glutamate transporter vGlut1 GABA hippocampus hypothalamus, controls. Immunoreactivity against GFAP and/or Iba-1 was higher than suggesting occurrence gliosis. We conclude distinct neurochemical brain.

Language: Английский

Citations

107

Oxidative Stress and Inflammation Interdependence in Multiple Sclerosis DOI Open Access
Rodica Pădureanu, Carmen Valeria Albu, Radu Răzvan Mititelu

et al.

Journal of Clinical Medicine, Journal Year: 2019, Volume and Issue: 8(11), P. 1815 - 1815

Published: Nov. 1, 2019

The study aims to explore the oxidative status related inflammation in peripheral blood of stable relapsing-remitting multiple sclerosis (MS) patients with low disability. In this study, 31 people were included and divided into two groups: an MS group which 16 a disability level (age 38.9 ± 7.08, EDSS median 2.5) control that contains 15 healthy volunteers similar age group. Thiobarbituric acid reactive substances (TBARS), protein carbonyl (PCO), total antioxidant capacity (TAC) as stress markers, neutrophil/lymphocyte ratio (NLR), erythrocyte sedimentation rate (ESR) analyzed sample establish stress/inflammatory using conventional plasma markers. we showed pro-inflammatory relapse-remitting stage diseases can be easily accurately appreciated by NLR. An increased NLR is associated decreased capacity, even early neuronal damage. Oxidative aggravates functional outcome, potentiates damage, accelerate progression disease.

Language: Английский

Citations

103

Fatty Acids: An Insight into the Pathogenesis of Neurodegenerative Diseases and Therapeutic Potential DOI Open Access
Diego Julián Vesga-Jiménez,

Cynthia Martin,

George E. Barreto

et al.

International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(5), P. 2577 - 2577

Published: Feb. 25, 2022

One of the most common lipids in human body is palmitic acid (PA), a saturated fatty with essential functions brain cells. PA used by cells as an energy source, besides being precursor signaling molecules and protein tilting across membrane. Although plays physiological brain, its excessive accumulation leads to detrimental effects on cells, causing lipotoxicity. This mechanism involves activation toll-like receptors (TLR) nuclear factor kappa-light-chain-enhancer activated B (NF-κB) pathways, consequent release pro-inflammatory cytokines, increased production reactive oxygen species (ROS), endoplasmic reticulum (ER) stress, autophagy impairment. Importantly, some cellular changes induced lead augmented susceptibility development Alzheimer’s Parkinson´s diseases. Considering complexity response intrinsic differences this review, we provide overview molecular different their possible relationships neurodegenerative diseases (NDs). Furthermore, propose use other acids, such oleic or linoleic acid, potential therapeutic approaches against NDs, these acids can counteract PA’s negative

Language: Английский

Citations

48

Metabolic defects shared by Alzheimer's disease and diabetes: A focus on mitochondria DOI Creative Commons
Cristina Carvalho, Paula I. Moreira

Current Opinion in Neurobiology, Journal Year: 2023, Volume and Issue: 79, P. 102694 - 102694

Published: Feb. 24, 2023

Type 2 diabetes (T2D) and Alzheimer's disease (AD) are two global epidemics that share several metabolic defects, such as insulin resistance, impaired glucose metabolism, mitochondrial defects. Importantly, strong evidence demonstrates T2D significantly increases the risk of cognitive decline dementia, particularly AD. Here, we provide an overview defects characterize link both pathologies putting focus on mitochondria. The biomarker potential components therapeutic some drugs target modulate mitochondria also briefly discussed.

Language: Английский

Citations

29

The roles of dietary polyphenols at crosstalk between type 2 diabetes and Alzheimer's disease in ameliorating oxidative stress and mitochondrial dysfunction via PI3K/Akt signaling pathways DOI

Jingwen Wang,

Jingyang Zhang, Zhi‐Ling Yu

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 99, P. 102416 - 102416

Published: July 13, 2024

Language: Английский

Citations

13