The Effect of Resveratrol on Neurodegenerative Disorders: Possible Protective Actions Against Autophagy, Apoptosis, Inflammation and Oxidative Stress

2019 ◽  
Vol 25 (19) ◽  
pp. 2178-2191 ◽  
Author(s):  
Mohammad H. Pourhanifeh ◽  
Rana Shafabakhsh ◽  
Russel J. Reiter ◽  
Zatollah Asemi
Keyword(s):  
Oxidative Stress ◽  
Neurodegenerative Disorders ◽  
Cell Damage ◽  
Current Evidence ◽  
Therapeutic Effects ◽  
Neuronal Function ◽  
Beneficial Effects ◽  
Cellular Processes ◽  
And Oxidative Stress

The prevalence of neurodegenerative disorders characterized by the loss of neuronal function is rapidly increasing. The pathogenesis of the majority of these diseases is not entirely clear, but current evidence has shown the possibility that autophagy, apoptosis, inflammation and oxidative stress are involved. The present review summarizes the therapeutic effects of resveratrol on neurodegenerative disorders, based on the especially molecular biology of these diseases. The PubMed, Cochrane, Web of Science and Scopus databases were searched for studies published in English until March 30th, 2019 that contained data for the role of inflammation, oxidative stress, angiogenesis and apoptosis in the neurodegenerative disorders. There are also studies documenting the role of molecular processes in the progression of central nervous system diseases. Based on current evidence, resveratrol has potential properties that may reduce cell damage due to inflammation. This polyphenol affects cellular processes, including autophagy and the apoptosis cascade under stressful conditions. Current evidence supports the beneficial effects of resveratrol on the therapy of neurodegenerative disorders.

scholarly journals The Golgi apparatus in neurorestoration

2019 ◽  
Vol 7 (3) ◽  
pp. 116-128
Author(s):  
Jianyang Liu ◽  
Jialin He ◽  
Yan Huang ◽  
Han Xiao ◽  
Zheng Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Golgi Apparatus ◽  
Neurodegenerative Diseases ◽  
Disease Progression ◽  
Neurological Recovery ◽  
Cellular Processes ◽  
Wide Range ◽  
And Oxidative Stress

The central role of the Golgi apparatus in critical cellular processes such as the transport, processing, and sorting of proteins and lipids has placed it at the forefront of cell science. Golgi apparatus dysfunction caused by primary defects within the Golgi or pharmacological and oxidative stress has been implicated in a wide range of neurodegenerative diseases. In addition to participating in disease progression, the Golgi apparatus plays pivotal roles in angiogenesis, neurogenesis, and synaptogenesis, thereby promoting neurological recovery. In this review, we focus on the functions of the Golgi apparatus and its mediated events during neurorestoration.

Beneficial effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin in rats

2015 ◽  
Vol 35 (3) ◽  
pp. 276-281 ◽  
Author(s):  
H Elbe ◽  
Z Dogan ◽  
E Taslidere ◽  
A Cetin ◽  
Y Turkoz
Keyword(s):  
Oxidative Stress ◽  
Renal Injury ◽  
Kidney Tissue ◽  
Albino Rats ◽  
Therapeutic Effects ◽  
Histopathological Changes ◽  
Tubular Atrophy ◽  
Beneficial Effects ◽  
Wistar Albino Rats ◽  
And Oxidative Stress

Ciprofloxacin is a broad-spectrum quinolone antibiotic commonly used in clinical practice. Quercetin is an antioxidant belongs to flavonoid group. It inhibits the production of superoxide anion. In this study, we aimed to evaluate the effects of quercetin on renal injury and oxidative stress caused by ciprofloxacin. Twenty-eight female Wistar albino rats were divided into four groups: control, quercetin (20 mg kg−1 day−1 gavage for 21 days), ciprofloxacin (20 mg kg−1 twice a day intraperitoneally for 10 days), and ciprofloxacin + quercetin. Samples were processed for histological and biochemical evaluations. Malondialdehyde (MDA) and glutathione (GSH) levels, superoxide dismutase (SOD), and catalase (CAT) activities were measured in kidney tissue. The ciprofloxacin group showed histopathological changes such as infiltration, dilatation in tubules, tubular atrophy, reduction of Bowman’s space, congestion, hemorrhage, and necrosis. In the ciprofloxacin + quercetin group, these histopathological changes markedly reduced. MDA levels increased in the ciprofloxacin group and decreased in the ciptofloxacin + quercetin group. SOD and CAT activities and GSH levels significantly decreased in the ciprofloxacin group. On the other hand, in the ciprofloxacin + quercetin group, SOD and CAT activities and GSH levels significantly increased with regard to the ciprofloxacin group. We concluded that quercetin has antioxidative and therapeutic effects on renal injury and oxidative stress caused by ciprofloxacin in rats.

scholarly journals New Insights in the Pathogenesis of HPV Infection and the Associated Carcinogenic Processes: The Role of Chronic Inflammation and Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Simona Roxana Georgescu ◽  
Cristina Iulia Mitran ◽  
Madalina Irina Mitran ◽  
Constantin Caruntu ◽  
Maria Isabela Sarbu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Cell Damage ◽  
Redox Homeostasis ◽  
Harmful Effect ◽  
Hpv Infection ◽  
Host Cells ◽  
E6 And E7 ◽  
And Oxidative Stress

Human papillomavirus (HPV) is a small double-stranded DNA virus with tropism for epithelial cells. To this date, over 150 genotypes are known and are classified into two major groups, low-risk and high-risk strains, depending on the ability of the virus to induce malignant transformation. The host’s immunity plays a central role in the course of the infection; therefore, it may not be clinically manifest or may produce various benign or malignant lesions. The pathogenic mechanisms are complex and incompletely elucidated. Recent research suggests the role of chronic inflammation and oxidative stress (OS) in the pathogenesis of HPV infection and the associated carcinogenic processes. Chronic inflammation induces OS, which in turn promotes the perpetuation of the inflammatory process resulting in the release of numerous molecules which cause cell damage. Reactive oxygen species exert a harmful effect on proteins, lipids, and nucleic acids. Viral oncogenes E5, E6, and E7 are involved in the development of chronic inflammation through various mechanisms. In addition, HPV may interfere with redox homeostasis of host cells, inducing OS which may be involved in the persistence of the infection and play a certain role in viral integration and promotion of carcinogenesis. Knowledge regarding the interplay between chronic inflammation and OS in the pathogenesis of HPV infection and HPV-induced carcinogenesis has important consequences on the development of new therapeutic strategies.

scholarly journals NLRP3 inflammasome mediates oxidative stress-induced pancreatic islet dysfunction

2018 ◽  
Vol 315 (5) ◽  
pp. E912-E923 ◽  
Author(s):  
Marina Sokolova ◽  
Afaf Sahraoui ◽  
Merete Høyem ◽  
Jonas Øgaard ◽  
Egil Lien ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Nlrp3 Inflammasome ◽  
Ex Vivo ◽  
Cell Damage ◽  
Macrophage Infiltration ◽  
Β Cell ◽  
Beneficial Effects ◽  
Islet Dysfunction

Inflammasomes are multiprotein inflammatory platforms that induce caspase-1 activation and subsequently interleukin (IL)-1β and IL-18 processing. The NLRP3 inflammasome is activated by different forms of oxidative stress, and, based on the central role of IL-1β in the destruction of pancreatic islets, it could be related to the development of diabetes. We therefore investigated responses in wild-type C57Bl/6 (WT) mice, NLRP3−/− mice, and mice deficient in apoptosis-associated speck-like protein containing a caspase-recruitment domain (ASC) after exposing islets to short-term hypoxia or alloxan-induced islet damage. NLRP3-deficient islets compared with WT islets had preserved function ex vivo and were protected against hypoxia-induced cell death. Furthermore, NLRP3 and ASC-deficient mice were protected against oxidative stress-induced diabetes caused by repetitive low-dose alloxan administration, and this was associated with reduced β-cell death and reduced macrophage infiltration. This suggests that the beneficial effect of NLRP3 inflammasome deficiency on oxidative stress-mediated β-cell damage could involve reduced macrophage infiltration and activation. To support the role of macrophage activation in alloxan-induced diabetes, we injected WT mice with liposomal clodronate, which causes macrophage depletion before induction of a diabetic phenotype by alloxan treatment, resulting in improved glucose homeostasis in WT mice. We show here that the NLRP3 inflammasome acts as a mediator of hypoxia and oxidative stress in insulin-producing cells, suggesting that inhibition of the NLRP3 inflammasome could have beneficial effects on β-cell preservation.

scholarly journals Exploring Biologic Correlates of Cancer-Related Fatigue in Men With Prostate Cancer: Cell Damage Pathways and Oxidative Stress

2020 ◽  
Vol 22 (4) ◽  
pp. 514-519
Author(s):  
Kristin Dickinson ◽  
Adam J. Case ◽  
Kevin Kupzyk ◽  
Leorey Saligan
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Potential Role ◽  
Cell Damage ◽  
Cellular Responses ◽  
Preliminary Evidence ◽  
Cancer Related Fatigue ◽  
Targeted Treatments ◽  
And Oxidative Stress

The pathobiology of cancer-related fatigue (CRF) remains elusive, hindering the development of targeted treatments. Radiation therapy (RT), a common treatment for men with prostate cancer, induces cell damage through the generation of free radicals and oxidative stress. We hypothesized that disruption in cellular responses to this surge of nonphysiological oxidative stress might contribute to CRF in men with prostate cancer treated with RT. We evaluated the potential role of three cell damage pathways (apoptosis, autophagy, necrosis) and oxidative stress in CRF in men with prostate cancer receiving RT. Fatigue was measured by the Functional Assessment of Cancer Therapy-Fatigue (FACT-F) questionnaire. Gene expression was measured in whole blood using RT2 profiler™ PCR arrays. Data were collected at two time points: either baseline or Day 1 of treatment (T1) and completion of treatment (T2). Participants were grouped into either the fatigued or nonfatigued phenotype at T2 using the recommended FACT-F cut-off score for clinical significance. We observed significant upregulation of seven genes related to three cell damage pathways in the fatigued group from T1 to T2 and no significant changes in the nonfatigued group. We also observed significant downregulation of two genes related to oxidative stress in the fatigued group compared to the nonfatigued group at T2. These collective results provide preliminary evidence that cell damage might be upregulated in the CRF phenotype. Validation of these findings using a larger and more diverse sample is warranted.

scholarly journals Sepsis and Oxidative Stress in the Newborn: From Pathogenesis to Novel Therapeutic Targets

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Chiara Poggi ◽  
Carlo Dani
Keyword(s):  
Oxidative Stress ◽  
Neonatal Sepsis ◽  
Cell Damage ◽  
Cellular Damage ◽  
Antioxidant Systems ◽  
Adjunct Treatment ◽  
Beneficial Effects ◽  
Redox Cycles ◽  
Antioxidant Agents ◽  
And Oxidative Stress

Sepsis is at present one of the leading causes of morbidity and mortality in the neonatal population. Together with inflammation, oxidative stress is involved in detrimental pathways activated during neonatal sepsis, eventually leading to organ dysfunction and death. The redox cascade during sepsis is mainly initiated by IL-6 and IL-8 stimulation in newborns and includes multiple noxious processes, as direct cell damage induced by reactive oxygen species, activation of gene expression leading to amplification of inflammation and oxidative stress, and impairment of mitochondrial function. Once proinflammatory and prooxidant pathways are established as stimulated by causing pathogens, self-maintaining unfavorable redox cycles ensue, leading to oxidative stress-related cellular damage, independently from the activating pathogens themselves. Despite antioxidant systems are induced during neonatal sepsis, as an adaptive response to an increased oxidative burden, a condition of redox imbalance favoring oxidative pathways occurs, resulting in increased markers of oxidative stress damage. Therefore, antioxidant treatment would exert beneficial effects during neonatal sepsis, potentially interrupting prooxidant pathways and preventing the maintenance of detrimental redox cycles that cannot be directly affected by antibiotic treatment. Among others, antioxidant agents investigated in clinical settings as adjunct treatment for neonatal sepsis include melatonin and pentoxifylline, both showing promising results, while novel antioxidant molecules, as edaravone and endothelin receptor antagonists, are at present under investigation in animal models. Finally, mitochondria-targeted antioxidant treatments could represent an interesting line of research in the treatment of neonatal sepsis.

scholarly journals Unveiling the Role of Inflammation and Oxidative Stress on Age-Related Cardiovascular Diseases

2020 ◽  
Vol 2020 ◽  
pp. 1-20 ◽  
Author(s):  
Arthur José Pontes Oliveira de Almeida ◽  
Mathania Silva de Almeida Rezende ◽  
Sabine Helena Dantas ◽  
Sonaly de Lima Silva ◽  
Júlio César Pinheiro Lúcio de Oliveira ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Diseases ◽  
Inflammatory Process ◽  
Cell Damage ◽  
Stressful Environment ◽  
Age Related ◽  
Cellular Components ◽  
Global Population ◽  
And Oxidative Stress

The global population above 60 years has been growing exponentially in the last decades, which is accompanied by an increase in the prevalence of age-related chronic diseases, highlighting cardiovascular diseases (CVDs), such as hypertension, atherosclerosis, and heart failure. Aging is the main risk factor for these diseases. Such susceptibility to disease is explained, at least in part, by the increase of oxidative stress, in which it damages cellular components such as proteins, DNA, and lipids. In addition, the chronic inflammatory process in aging “inflammaging” also contributes to cell damage, creating a stressful environment which drives to the development of CVDs. Taken together, it is possible to identify the molecular connection between oxidative stress and the inflammatory process, especially by the crosstalk between the transcription factors Nrf-2 and NF-κB which are mediated by redox signalling and are involved in aging. Therapies that control this process are key targets in the prevention/combat of age-related CVDs. In this review, we show the basics of inflammation and oxidative stress, including the crosstalk between them, and the implications on age-related CVDs.

scholarly journals The Involvement of the Oxidative Stress Status in Cancer Pathology: A Double View on the Role of the Antioxidants

2021 ◽  
Vol 2021 ◽  
pp. 1-25
Author(s):  
Kamal Fatima Zahra ◽  
Radu Lefter ◽  
Ahmad Ali ◽  
Ech-Chahad Abdellah ◽  
Constantin Trus ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Harmful Effect ◽  
Phagocytic Cells ◽  
Beneficial Effects ◽  
Cellular Processes ◽  
Cancer Pathology ◽  
Potential Biomarker ◽  
Oxidative Stress Status ◽  
Risk Of Cancer

Oxygen-free radicals, reactive oxygen species (ROS) or reactive nitrogen species (RNS), are known by their “double-sided” nature in biological systems. The beneficial effects of ROS involve physiological roles as weapons in the arsenal of the immune system (destroying bacteria within phagocytic cells) and role in programmed cell death (apoptosis). On the other hand, the redox imbalance in favor of the prooxidants results in an overproduction of the ROS/RNS leading to oxidative stress. This imbalance can, therefore, be related to oncogenic stimulation. High levels of ROS disrupt cellular processes by nonspecifically attacking proteins, lipids, and DNA. It appears that DNA damage is the key player in cancer initiation and the formation of 8-OH-G, a potential biomarker for carcinogenesis. The harmful effect of ROS is neutralized by an antioxidant protection treatment as they convert ROS into less reactive species. However, contradictory epidemiological results show that supplementation above physiological doses recommended for antioxidants and taken over a long period can lead to harmful effects and even increase the risk of cancer. Thus, we are describing here some of the latest updates on the involvement of oxidative stress in cancer pathology and a double view on the role of the antioxidants in this context and how this could be relevant in the management and pathology of cancer.

scholarly journals Glutathione and Catalase Provide Overlapping Defenses for Protection against Respiration-Generated Hydrogen Peroxide in Haemophilus influenzae

2003 ◽  
Vol 185 (18) ◽  
pp. 5555-5562 ◽  
Author(s):  
Bjorn Vergauwen ◽  
Frederik Pauwels ◽  
Jozef J. Van Beeumen
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Haemophilus Influenzae ◽  
Growth Medium ◽  
Primary System ◽  
Aerobic Growth ◽  
Cellular Processes ◽  
Defense Systems ◽  
And Oxidative Stress

ABSTRACT Glutathione is an abundant and ubiquitous low-molecular-weight thiol that may play a role in many cellular processes, including protection against the deleterious effects of reactive oxygen species. We address here the role of glutathione in protection against hydrogen peroxide (H2O2) in Haemophilus influenzae and show that glutathione and catalase provide overlapping defense systems. H. influenzae is naturally glutathione deficient and imports glutathione from the growth medium. Mutant H. influenzae lacking catalase and cultured in glutathione-deficient minimal medium is completely devoid of H2O2 scavenging activity and, accordingly, substantial amounts of H2O2 accumulate in the growth medium. H. influenzae generates H2O2 at rates similar to those reported for Escherichia coli, but the toxicity of this harmful metabolite is averted by glutathione-based H2O2 removal, which appears to be the primary system for protection against H2O2 endogenously generated during aerobic respiration. When H2O2 concentrations exceed low micromolar levels, the hktE gene-encoded catalase becomes the predominant scavenger. The requirement for glutathione in protection against oxidative stress is analogous to that in higher and lower eukaryotes but is unlike the situation in other bacteria in which glutathione is dispensable for aerobic growth during both normal and oxidative stress conditions.

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