scholarly journals Reappraisal of Dietary Phytochemicals for Coronavirus Infection: Focus on Hesperidin and Quercetin

2021 ◽  
Author(s):  
Paolo Bellavite
Keyword(s):  
Oxidative Stress ◽  
Infectious Diseases ◽  
Proteolytic Enzymes ◽  
Antimicrobial Properties ◽  
Large Family ◽  
Cellular Level ◽  
Activation Mechanism ◽  
In Silico Simulation ◽  
Infection Focus ◽  
Cellular Defence

Food polyphenols constitute a large family of substances with beneficial properties in a large group of communicable and non-communicable diseases. These compounds support and improve the body’s defences against oxidative stress and are helpful in the prevention of pathologies related to metabolic syndrome. Furthermore, they exhibit anti-inflammatory, antiviral, and antimicrobial properties. This chapter draws attention to certain nutritional components such as hesperidin and quercetin, which are emerging as good candidates for a complementary beneficial effect in the case of diseases caused by viruses, including COVID-19. These nutraceuticals have a complex mechanism of action, which involves both cellular defence against oxidative stress and the modulation of inflammation, which although normally is a defence, repair and activation mechanism of the immune system, it can elude its controls and become a systemic and destructive pathology (cytokine storm, respiratory distress syndrome). Furthermore, recent in silico simulation tests suggest that both hesperidin and quercetin may interfere with SARS-CoV-2 by binding to cell receptors and the proteolytic enzymes involved in its replication. In addition to the inhibitory effects on the virus at cellular level, the two flavonoids can have indirect effects in respiratory infectious diseases as they prevent or improve metabolic and vascular comorbidities that can complicate the clinical course. This brief review focuses on biochemical and pharmacological mechanisms of action of polyphenols in the context of the revaluation of dietary approaches to the prevention and treatment of infectious diseases caused by viruses, with a special application to COVID-19.

Exploiting Anti-Inflammation Effects of Flavonoids in Chronic Inflammatory Diseases

2020 ◽  
Vol 26 (22) ◽  
pp. 2610-2619 ◽  
Author(s):  
Tarique Hussain ◽  
Ghulam Murtaza ◽  
Huansheng Yang ◽  
Muhammad S. Kalhoro ◽  
Dildar H. Kalhoro
Keyword(s):  
Oxidative Stress ◽  
Chronic Diseases ◽  
Inflammatory Diseases ◽  
Therapeutic Option ◽  
Cellular Level ◽  
Antiinflammatory Drugs ◽  
Suitable Alternative ◽  
Chronic Inflammatory Diseases

Background: Inflammation is a complex response of the host defense system to different internal and external stimuli. It is believed that persistent inflammation may lead to chronic inflammatory diseases such as, inflammatory bowel disease, neurological and cardiovascular diseases. Oxidative stress is the main factor responsible for the augmentation of inflammation via various molecular pathways. Therefore, alleviating oxidative stress is effective a therapeutic option against chronic inflammatory diseases. Methods: This review article extends the knowledge of the regulatory mechanisms of flavonoids targeting inflammatory pathways in chronic diseases, which would be the best approach for the development of suitable therapeutic agents against chronic diseases. Results: Since the inflammatory response is initiated by numerous signaling molecules like NF-κB, MAPK, and Arachidonic acid pathways, their encountering function can be evaluated with the activation of Nrf2 pathway, a promising approach to inhibit/prevent chronic inflammatory diseases by flavonoids. Over the last few decades, flavonoids drew much attention as a potent alternative therapeutic agent. Recent clinical evidence has shown significant impacts of flavonoids on chronic diseases in different in-vivo and in-vitro models. Conclusion: Flavonoid compounds can interact with chronic inflammatory diseases at the cellular level and modulate the response of protein pathways. A promising approach is needed to overlook suitable alternative compounds providing more therapeutic efficacy and exerting fewer side effects than commercially available antiinflammatory drugs.

scholarly journals Complementary interactions between oxidative stress and auxins control plant growth responses at plant, organ, and cellular level

2005 ◽  
Vol 56 (418) ◽  
pp. 1991-2001 ◽  
Author(s):  
Taras Pasternak ◽  
Geert Potters ◽  
Roland Caubergs ◽  
Marcel A. K. Jansen
Keyword(s):  
Oxidative Stress ◽  
Plant Growth ◽  
Control Plant ◽  
Cellular Level ◽  
Growth Responses ◽  
Plant Organ ◽  
Complementary Interactions

scholarly journals Upregulation of Nrf2 expression by human cytomegalovirus infection protects host cells from oxidative stress

2013 ◽  
Vol 94 (7) ◽  
pp. 1658-1668 ◽  
Author(s):  
Junsub Lee ◽  
Kyungmi Koh ◽  
Young-Eui Kim ◽  
Jin-Hyun Ahn ◽  
Sunyoung Kim
Keyword(s):  
Oxidative Stress ◽  
Human Cytomegalovirus ◽  
Survival Rates ◽  
Buthionine Sulfoximine ◽  
Host Cells ◽  
Related Factor ◽  
Downstream Target ◽  
Human Foreskin Fibroblasts ◽  
Cellular Defence ◽  
Nrf2 Expression

NF-E2 related factor 2 (Nrf2) is a transcription factor that plays a key role(s) in cellular defence against oxidative stress. In this study, we showed that the expression of Nrf2 was upregulated in primary human foreskin fibroblasts (HFFs), following human cytomegalovirus (HCMV/HHV-5) infection. The expression of haem oxygenase-1, a downstream target of Nrf2, was also increased by HCMV infection, and this induction was suppressed in HFFs expressing a small hairpin RNA (shRNA) against Nrf2. The HCMV-mediated increase in Nrf2 expression was abolished when UV-irradiated virus was used or when the activity of casein kinase 2 was inhibited. Host cells infected by HCMV had higher survival rates following oxidative stress induced by buthionine sulfoximine compared with uninfected control cells, but this cell-protective effect was abolished by the use of Nrf2 shRNA. Our results suggest that HCMV-mediated activation of Nrf2 might be beneficial to the virus by increasing the host cell’s ability to cope with oxidative stress resulting from viral infection and/or inflammation.

scholarly journals Quality control in oocytes by p63 is based on a spring-loaded activation mechanism on the molecular and cellular level

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Daniel Coutandin ◽  
Christian Osterburg ◽  
Ratnesh Kumar Srivastav ◽  
Manuela Sumyk ◽  
Sebastian Kehrloesser ◽  
...  
Keyword(s):  
Dna Damage ◽  
Quality Control ◽  
Cellular Level ◽  
Activation Mechanism ◽  
Control Factor ◽  
Dna Double Strand Breaks ◽  
High Concentration ◽  
P53 Family ◽  
Strand Breaks ◽  
Induced Apoptosis

Mammalian oocytes are arrested in the dictyate stage of meiotic prophase I for long periods of time, during which the high concentration of the p53 family member TAp63α sensitizes them to DNA damage-induced apoptosis. TAp63α is kept in an inactive and exclusively dimeric state but undergoes rapid phosphorylation-induced tetramerization and concomitant activation upon detection of DNA damage. Here we show that the TAp63α dimer is a kinetically trapped state. Activation follows a spring-loaded mechanism not requiring further translation of other cellular factors in oocytes and is associated with unfolding of the inhibitory structure that blocks the tetramerization interface. Using a combination of biophysical methods as well as cell and ovary culture experiments we explain how TAp63α is kept inactive in the absence of DNA damage but causes rapid oocyte elimination in response to a few DNA double strand breaks thereby acting as the key quality control factor in maternal reproduction.

scholarly journals O Ensino da Antibioterapia: Estado da arte

2019 ◽  
Vol 20 ◽  
pp. 632-637
Author(s):  
Maria José Saavedraa ◽  
João Carlos Sousa
Keyword(s):  
Infectious Diseases ◽  
Large Scale ◽  
Action Plan ◽  
Antimicrobial Properties ◽  
Hospital Setting ◽  
Multidrug Resistant ◽  
World Health ◽  
Novel Approach ◽  
Paul Ehrlich ◽  
Alexander Fleming

Resumo A elevada mortalidade pelas doenças infecciosas, sobretudo epidémicas, mobilizou os cientistas na pesquisa de compostos naturais e produtos de síntese química dotados de propriedades antimicrobianas. Fazendo um pouco de história, referimos Paul Ehrlich, que utilizou o primeiro agente quimioterapêutico -Salvarsan, mais tarde Gerhard Domagk, que utilizou um pro-fármaco percursor de uma sulfamida. Em 1928, Alexander Fleming, descobriu de forma “casual” a penicilina, o primeiro antibiótico. Posteriormente em 1941 Howard Florey e Ernest Chain isolam e purificam a penicilina o que permitiu a sua utilização em larga escala -Era dos Antibióticos. A utilização dos antibióticos (AB) no tratamento das doenças infecciosas constituiu um dos maiores avanços da Medicina no séc. XX. No entanto a sua utilização em larga escala promoveu o aumento da incidência de estirpes multiresistentes aos AB, sobretudo em ambiente hospitalar. Adicionalmente verifica-se uma ocorrência cada vez mais elevada de estirpes resistentes na comunidade–humanos, animais e ambiente. O conhecimento dos mecanismos de ação e da ineficácia dos diferentes grupos farmacológicos de antibióticos é vital para o desenvolvimento de futuros microbianos, estando a ser estudados microrganismos do solo com a finalidade de encontrara novos fármacos. De realçar que a OMS preconiza que caminhamos rumo a uma "era pós-antibiótico”. Se não houver um plano de ação global para o "uso racional de antibióticos" a OMS prevê que em 2050 a resistência aos antibióticos, poderá matar mais de 10 milhões de pessoas.Palavras-chave: antibioterapia; resistência; antibióticos Abstract The current research on infectious diseases, especially with epidemic potential, has mobilized the scientific community to research on the natural substance and chemical probing products with antimicrobial properties. In a brief history of antibiotics, we refer to Paul Ehrlich, who used the first chemotherapeutic agent - Salvarsan, later Gerhard Domagk, who used a sulfamide precursor prodrug. In 1928 Alexander Fleming "casually" discovered penicillin, the first antibiotic. Later in 1941 Howard Florey and Ernest Chain isolate and purify penicillin that can be used on a large scale - Antibiotics Era. The use of antibiotics (AB) in the treatment of infectious diseases is one of the greatest advances of medicine in the 19th century. However, its large-scale use has increased the incidence of multidrug-resistant processes in AB, especially in a hospital setting. Besides, there is an increasing occurrence of resistant strains in different communities - humans, animals and in the environment. Understand the mechanisms of action and the ineffectiveness of the diverse pharmacological groups of antibiotics is crucial to provide further new antibiotic therapies in the near future. Recent studies have highlighted the soil-derived microorganisms as a novel approach to identify new drug substances. In this context, it is noteworthy that the World Health Organization (WHO) considers that we are moving towards a “post-antibiotic era”. If there is no global action plan for “rational use of antibiotics” WHO predicts that in 2050 the global impacts of antibiotic resistance on human heath will be catastrophic, killing more than 10 million people worldwide. Keywords: antibiotic therapy; resistence; antibiotics

scholarly journals Synergistic Effects of Curcumin and Nano-Curcumin against Toxicity, Carcinogenicity, and Oxidative Stress Induced by Tartrazine at Normal and Cancer Cell Levels

Catalysts ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1203
Author(s):  
Gaber E. El-Desoky ◽  
Saikh M. Wabaidur ◽  
Mohamed A. Habila ◽  
Zeid A. AlOthman
Keyword(s):  
Oxidative Stress ◽  
Synergistic Effects ◽  
Economic Benefits ◽  
Cellular Level ◽  
Anticancer Properties ◽  
Antioxidant Defense Enzymes ◽  
Apoptosis Protein ◽  
Nano Formulation

In this study, the cellular synergistic and antagonistic effects of mixing tartrazine (TZ) with curcumin (CUR) or curcumin-nanoparticles (CUR-NPs) were investigated. The in vivo administration of TZ, CUR, CUR-NPs, and TZ mixed with CUR or CUR-NPs at 75:25 or 50:50 ratios were tested. The results indicated that CUR and CUR -NPs reduced the cytotoxicity effects of TZ on skin fibroblast BJ-1 (ATCC® CRL-2522™) normal cells. However, among the tested materials, CUR-NPs had highest in vitro and in vivo antioxidant activity compared to TZ. Furthermore, CUR-NPs and CUR exhibited anticancer activity against HepG-2 liver cancer cells via apoptosis induction. The key apoptosis protein genes Caspase-3, p53, and Bax were upregulated, whereas Bc-2, which exhibits anti-apoptosis activity, was downregulated. Our results indicated that the nano-formulation of CUR alters its physicochemical properties, including the size and shape, and increases its antioxidant and anticancer properties. CUR-NPs also overcome the side effect of using TZ as a yellow color and food preservative additive, due to its reduced toxicity, oxidative stress, and carcinogenicity. In agreement with our previous findings, CUR and CUR-NPs were able to protect against cellular oxidative stress by stimulating endogenous antioxidant defense enzymes, including superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH), glutathione peroxidase (GPx), and glutathione-S-transferase (GST). We conclude that the nano-formulation of CUR exhibits economic benefits as a new strategy to use CUR as a food additive at the cellular level.

scholarly journals Emerging Roles of Redox-Mediated Angiogenesis and Oxidative Stress in Dermatoses

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Dehai Xian ◽  
Jing Song ◽  
Lingyu Yang ◽  
Xia Xiong ◽  
Rui Lai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Growth Factors ◽  
Molecular Mechanisms ◽  
Capillary Tube ◽  
Proteolytic Enzymes ◽  
Skin Tumor ◽  
Antioxidant Systems ◽  
Antiangiogenic Factors ◽  
And Oxidative Stress

Angiogenesis is the process of new vessel formation, which sprouts from preexisting vessels. This process is highly complex and primarily involves several key steps, including stimulation of endothelial cells by growth factors, degradation of the extracellular matrix by proteolytic enzymes, migration and proliferation of endothelial cells, and capillary tube formation. Currently, it is considered that multiple cytokines play a vital role in this process, which consist of proangiogenic factors (e.g., vascular endothelial growth factor, fibroblast growth factors, and angiopoietins) and antiangiogenic factors (e.g., endostatin, thrombospondin, and angiostatin). Angiogenesis is essential for most physiological events, such as body growth and development, tissue repair, and wound healing. However, uncontrolled neovascularization may contribute to angiogenic disorders. In physiological conditions, the above promoters and inhibitors function in a coordinated way to induce and sustain angiogenesis within a limited period of time. Conversely, the imbalance between proangiogenic and antiangiogenic factors could cause pathological angiogenesis and trigger several diseases. With insights into the molecular mechanisms of angiogenesis, increasing reports have shown that a close relationship exists between angiogenesis and oxidative stress (OS) in both physiological and pathological conditions. OS, an imbalance between prooxidant and antioxidant systems, is a cause and consequence of many vascular complains and serves as one of the biomarkers for these diseases. Furthermore, emerging evidence supports that OS and angiogenesis play vital roles in many dermatoses, such as psoriasis, atopic dermatitis, and skin tumor. This review summarizes recent findings on the role of OS as a trigger of angiogenesis in skin disorders, highlights newly identified mechanisms, and introduces the antiangiogenic and antioxidant therapeutic strategies.

Antioxidative effect of DJ-1 is enhanced in NG108-15 cells by DPMQ induced copper influx

2020 ◽  
Author(s):  
Ting-Yu Chin ◽  
Che-Chuan Wang ◽  
Kuo-Hsing Ma ◽  
Chia-Wei Kuo ◽  
Ming-Kuan Hu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Level ◽  
Nuclear Translocation ◽  
Cellular Level ◽  
Dependent Manner ◽  
Copper Binding ◽  
Antioxidative Effect ◽  
Sod Activity ◽  
Redox Imbalance ◽  
Endogenous Proteins

Disruption of copper homeostasis is closely involved in neurodegenerative disorders. This study examined whether a hybrid copper binding compound, (E)-2-(4-(dimethylamino)phenylimino)methyl)quinolin-8-ol (DPMQ), is able to protect NG108-15 cells against oxidative stress. we found that treatment of cells with rotenone or hydrogen peroxide increased cellular oxidative stress and resulted in mitochondrial dysfunction and apoptosis. The cellular levels of Nrf2 and the Cu2+ chaperone DJ-1 were also decreased. These oxidative detrimental effects were all inhibited when cells were co-treated with DPMQ. DPMQ increased cellular Cu2+ content, DJ-1 protein level, superoxide dismutase (SOD) activity and Nrf2 nuclear translocation under basal state. The activity of SOD decreased under redox imbalance and this decrease was blocked by DPMQ treatment, while the protein level of SOD1 remained unaltered regardless of the oxidative stress and DPMQ treatment. Using endogenous proteins, co-immunoprecipitation showed that DJ-1 bound with SOD1 and Nrf2 individually. The amount of Nrf2, bound to DJ-1, consistently reflected its cellular level, while the amount of SOD1, bound to DJ-1, was potentiated by DPMQ, being greater in basal state than under redox imbalance. Simultaneous inclusion of non-permeable Cu2+ chelator tetrathiomolybdate or triethylenetetramine during DPMQ treatment blocked all aforementioned effects of DPMQ, showing that the dependency of the effect of DPMQ on extracellular Cu2+. In addition, silencing of DJ-1 blocked the protection of DPMQ against oxidative stress. Taken all together, our results suggest that DPMQ stabilizes DJ-1 in a Cu2+ dependent manner, which then brings about SOD1 activation and Nrf2 nuclear translocation; these together alleviate cellular oxidative stress.

scholarly journals Natural Bioactive Compounds Acting against Oxidative Stress in Chronic, Degenerative, and Infectious Diseases

2018 ◽  
Vol 2018 ◽  
pp. 1-2 ◽  
Author(s):  
Roberto Mattioli ◽  
Luciana Mosca ◽  
Angel Sánchez-Lamar ◽  
Italo Tempera ◽  
Ralf Hausmann
Keyword(s):  
Oxidative Stress ◽  
Infectious Diseases ◽  
Bioactive Compounds

scholarly journals Low amounts of trans 18 : 1 fatty acids elevate plasma triacylglycerols but not cholesterol and alter the cellular defence to oxidative stress in mice

2005 ◽  
Vol 94 (3) ◽  
pp. 346-352 ◽  
Author(s):  
Nadège Cassagno ◽  
Antonio Palos-Pinto ◽  
Pierre Costet ◽  
Dominique Breilh ◽  
Michel Darmon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Rapeseed Oil ◽  
Fatty Acid Synthase ◽  
Hdl Cholesterol ◽  
Plasma Vitamin ◽  
Transfer Protein ◽  
Plasma Vitamin E ◽  
Cellular Defence

Trans fatty acids are found mainly in processed foods. It has been shown that when their intake is high, total cholesterol, LDL-cholesterol and triacylglycerols are elevated, while HDL-cholesterol decreases. To evaluate a possible effect of these compounds, even in low amounts, C57Bl/6J mice were fed for 7 weeks a diet containing 13·6 % energy as partially hydrogenated rapeseed oil-enriched diet (Trans diet). The Trans diet contained 3 % energy as trans 18 : 1 fatty acid (elaidic acid). Control mice were on an isologous diet containing native rapeseed oil (Rapeseed diet) in which trans fatty acids were undetectable. Total, free and HDL-cholesterol as well as reverse cholesterol transport did not change. However, plasma triacylglycerol and VLDL levels increased. Hepatic gene expression in the Trans v. Rapeseed diet were compared using quantitative RT–PCR. The Trans diet produced a 2–3-fold elevation in mRNA of fatty acid synthase and microsomal transfer protein mRNA, explaining (at least in part) the observed increase in triacylglycerols and VLDL. In addition, mice on the Trans diet developed a deficiency in plasma vitamin E accompanied by a higher concentration of F2-isoprostanes, indicative of increased oxidative stress. The 78 kDa glucose-related protein (GRP78) mRNA expression increased 3–4-fold in liver, suggesting that a response against apoptosis was provoked by lipid peroxidation.

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