Insulin Resistance and Oxidative Stress in the Brain: What’s New?

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

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Sources of free radicals and oxidative stress in the oral cavity

Archives of Oral Biology, Journal Year: 2018, Volume and Issue: 92, P. 8 - 17

Published: May 1, 2018

Language: Английский

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Alzheimer’s Disease as Type 3 Diabetes: Common Pathophysiological Mechanisms between Alzheimer’s Disease and Type 2 Diabetes

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

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Exploring the role of antioxidants in sepsis-associated oxidative stress: a comprehensive review

Frontiers in Cellular and Infection Microbiology, Journal Year: 2024, Volume and Issue: 14

Published: March 6, 2024

Sepsis is a potentially fatal condition characterized by organ dysfunction caused an imbalanced immune response to infection. Although increased inflammatory significantly contributes the pathogenesis of sepsis, several molecular mechanisms underlying progression sepsis are associated with cellular reactive oxygen species (ROS) generation and exhausted antioxidant pathways. This review article provides comprehensive overview involvement ROS in pathophysiology potential application antioxidants antimicrobial properties as adjunct primary therapies (fluid antibiotic therapies) against sepsis. delves into advantages disadvantages utilization therapeutic approach which has been explored variety animal models clinical trials. While suggested therapy suppress cases where intensified reaction occurs, use multiple agents can be beneficial they act additively or synergistically on different pathways, thereby enhancing defense. Furthermore, immunoadjuvant therapy, specifically septic patients displaying immunosuppressive tendencies, represents promising advancement therapy.

Language: Английский

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Oxidative stress biomarkers in the serum and plasma of patients with non-alcoholic fatty liver disease (NAFLD). Can plasma AGE be a marker of NAFLD? Oxidative stress biomarkers in NAFLD patients

Free Radical Research, Journal Year: 2019, Volume and Issue: 53(8), P. 841 - 850

Published: June 25, 2019

Still little is known about the redox abnormalities in patients with non-alcoholic fatty liver disease (NAFLD). The purpose of study was to find relationship between enzymatic and non-enzymatic antioxidants, homeostasis oxidative damage 67-patients NAFLD. population divided into (early NAFLD, n = 29) steatohepatitis (advanced 38). Redox biomarkers: antioxidants (Cu - Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), reductase (GR)); status (reduced (GSH), total antioxidant capacity (TAC)); products (total oxidant (TOS), advanced glycation end (AGE), malondialdehyde (MDA), DNA/RNA damage) were determined serum/plasma samples. activity SOD, GPx, GR levels GSH, TOS, AGE, MDA, significantly elevated early NAFLD group compared controls (p < .001). There a positive correlation TAC ALT (R 0.34, p .04; R 0.36, .03, respectively) group. Interestingly, ROC analysis for AGE showed good discriminatory ratio minimal steatosis (BARD score 0-1) vs. moderate 2-4), AUC 0.76. Plasma can be potential non-invasive biomarker differentiating patients.

Language: Английский

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Redox Balance, Antioxidant Defense, and Oxidative Damage in the Hypothalamus and Cerebral Cortex of Rats with High Fat Diet‐Induced Insulin Resistance

Oxidative Medicine and Cellular Longevity, Journal Year: 2018, Volume and Issue: 2018(1)

Published: Jan. 1, 2018

Oxidative stress is a key pathogenic factor in both neurogenerative and metabolic diseases. However, its contribution the brain complications of insulin resistance still not well understood. Therefore, aim this study was evaluation redox homeostasis oxidative damage hypothalamus cerebral cortex insulin-resistant control rats. 16 male Wistar rats were divided into two equal groups (n = 8): high fat diet group (HFD). Prooxidant enzymes (xanthine oxidase NADPH oxidase); enzymatic nonenzymatic antioxidants [glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), superoxide dismutase-1 (SOD-1), uric acid (UA)]; products [advanced glycation end (AGE), 4-hydroxynonenal (4-HNE), malondialdehyde (MDA), 8-hydroxy-2'-deoxyguanosine (8-OHdG)] as total antioxidant capacity (TAC), oxidant status (TOS), index (OSI), ferric reducing ability sample (FRAP) evaluated serum/plasma HFD-fed The activity prooxidant significantly increased vs. Additionally, we have showed enhanced efficiency (↑CAT, ↑UA, ↑TAC, ↑FRAP) (↑GPx, ↑CAT, ↑SOD-1, All markers (AGE, 4-HNE, MDA, 8-OHdG, OSI) rats, while only 4-HNE MDA markedly higher HFD group. Summarizing, results our indicate an adaptive response to production free radicals under conditions. Despite increase antioxidative defense systems, mechanism does protect structures from damages. more susceptible caused by HFD.

Language: Английский

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Antioxidant therapies in traumatic brain injury

Neurochemistry International, Journal Year: 2021, Volume and Issue: 152, P. 105255 - 105255

Published: Dec. 13, 2021

Language: Английский

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Fangchinoline diminishes STAT3 activation by stimulating oxidative stress and targeting SHP-1 protein in multiple myeloma model

Journal of Advanced Research, Journal Year: 2021, Volume and Issue: 35, P. 245 - 257

Published: March 21, 2021

The development of cancer generally occurs as a result various deregulated molecular mechanisms affecting the genes that can control normal cellular growth. Signal transducer and activator transcription 3 (STAT3) pathway, once aberrantly activated promote carcinogenesis by regulating number oncogenic genes.Here, we evaluated impact fangchinoline (FCN) to attenuate tumor growth survival through modulation STAT3 signaling pathway using diverse cell lines xenograft mouse model.To evaluate action FCN on cascade, protein levels were analyzed Western blot analysis electrophoretic mobility shift assay (EMSA). Translocation was detected immunocytochemistry. Thereafter, FCN-induced ROS measured GSH/GSSG H2DCF-DA. apoptosis flow cytometry for assays. Finally, anti-cancer effects in vivo myeloma model.We noted abrogated expression upstream signals (JAK1/2 Src). In addition, also attenuated DNA binding ability its translocation into nucleus. It altered proteins, increased SHP-1 levels, induced substantial U266 cells. promoted an production reactive oxygen species (ROS) GSSG/GSH ratio Moreover, effectively progression activation preclinical model.Overall, this study suggests may have tremendous potential alter abnormal induce death malignant cells along with causing suppression pathogenesis pro-oxidant dependent mechanism.

Language: Английский

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Eight-Week Consumption of High-Sucrose Diet Has a Pro-Oxidant Effect and Alters the Function of the Salivary Glands of Rats

Nutrients, Journal Year: 2018, Volume and Issue: 10(10), P. 1530 - 1530

Published: Oct. 17, 2018

A high-sucrose diet (HSD) is widely known for its cariogenic effects and promotion of obesity, insulin resistance, type 2 diabetes, cancer. However, the impact HSD on salivary gland function as well level oxidative stress still unknown requires evaluation. Our study first to determine both redox balance injury in parotid submandibular glands rats fed compared control group. We have demonstrated that uric acid concentration activity superoxide dismutase peroxidase varied significantly vs. enhanced damage proteins, lipids, DNA (increase advanced glycation end products, oxidation protein 4-hydroxynonenal, 8-hydroxy-2’-deoxyguanosine) was observed only rats. Moreover, also reduced total content amylase types decreased stimulated flow rate. To sum up, an reduces disturbs glands. are more vulnerable antioxidant disturbances damage.

Language: Английский

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The Impact of High-Fat Diet on Mitochondrial Function, Free Radical Production, and Nitrosative Stress in the Salivary Glands of Wistar Rats

Oxidative Medicine and Cellular Longevity, Journal Year: 2019, Volume and Issue: 2019, P. 1 - 15

Published: July 4, 2019

Oxidative stress plays a crucial role in the salivary gland dysfunction insulin resistance; however, cause of increased free radical formation these conditions is still unknown. Therefore, aim study was to investigate effect high-fat diet (HFD) on mitochondrial respiratory system, prooxidant enzymes, ROS production, and nitrosative/oxidative submandibular parotid glands rats. The experiment performed male Wistar rats divided into two groups (n = 10): control HFD. 8-week feeding HFD affects glucose metabolism observed as significant increase plasma well HOMA-IR compared activity Complex I II+III significantly decreased Mitochondrial cytochrome c oxidase (COX) hydrogen peroxide level were group those controls. also showed lower reduced glutathione (GSH) : oxidized (GSH GSSG) ratio, higher GSSG NADPH oxidase, xanthine levels oxidative/nitrosative (malonaldehyde, nitric oxide, nitrotyrosine, peroxynitrite) inflammation/apoptosis (interleukin-1β caspase-3) biomarkers statistically elevated comparison impairs function both types by enhancing stimulating inflammation apoptosis. However, protein nitration, lipid peroxidation more pronounced

Language: Английский

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