Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 November 2020) | Viewed by 80211

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Special Issue Editor

Special Issue Information

Dear Colleagues,

Oxidative stress and inflammation are two phenomena that are directly involved in practically all pathologies and especially in aging. However, they are not only involved in processes associated with damage. For instance, oxidative stress, which is associated with the redox state, constitutes an important mechanism in many physiological processes, such as adaptations to physical exercise, cell signaling, and hypothalamic regulation of appetite. Regarding inflammatory mediators, it is also known that they are essential in mechanisms such as the generation of gastric mucus for the protection of the stomach and the repair of tissues via the mobilization of stem cells. However, when these two phenomena are deregulated, their action is harmful. In this Special Issue, we ask ourselves several questions: How and when should we allow or block oxidative stress and inflammation? What is the advisable dose of antioxidant or anti-inflammatory therapy associated with aging? Are diet, physical exercise, and decreased psychological stress the best therapies for oxidative stress and inflammation control?

Prof. Dr. Juan Gambini
Guest Editor

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Keywords

  • oxidative stress
  • inflammation
  • molecular mechanisms
  • pharmacotherapy
  • diet
  • physical exercise
  • psychological stress
  • longevity
  • aging

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Published Papers (15 papers)

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Editorial

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5 pages, 201 KiB  
Editorial
Oxidative Stress and Inflammation: From Mechanisms to Therapeutic Approaches
by Juan Gambini and Kristine Stromsnes
Biomedicines 2022, 10(4), 753; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines10040753 - 23 Mar 2022
Cited by 6 | Viewed by 2481
Abstract
Oxidative stress and inflammation are two phenomena that are directly involved in practically all pathologies and especially in aging [...] Full article

Research

Jump to: Editorial, Review

10 pages, 1717 KiB  
Article
Antioxidant/Anti-Inflammatory Effects of Caloric Restriction in an Aged and Obese Rat Model: The Role of Adiponectin
by Daniele La Russa, Alessandro Marrone, Maurizio Mandalà, Rachele Macirella and Daniela Pellegrino
Biomedicines 2020, 8(12), 532; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8120532 - 25 Nov 2020
Cited by 23 | Viewed by 3631
Abstract
Caloric restriction (CR) represents a powerful intervention for extending healthspan and lifespan in several animal models, from yeast to primates. Additionally, in humans, CR has been found to induce cardiometabolic adaptations associated with improved health. In this study, we evaluated in an aged [...] Read more.
Caloric restriction (CR) represents a powerful intervention for extending healthspan and lifespan in several animal models, from yeast to primates. Additionally, in humans, CR has been found to induce cardiometabolic adaptations associated with improved health. In this study, we evaluated in an aged and obese rat model the effect of long-term (6 months) caloric restriction (−40%) on the oxidative/inflammatory balance in order to investigate the underlining mechanisms. In plasma, we analyzed the oxidative balance by photometric tests and the adiponectin/tumor necrosis factor-α-induced gene/protein 6 (TSG-6) levels by Western blot analysis. In the white adipose tissue, we examined the protein levels of AdipoR1, pAMPK, NFκB, NRF-2, and glutathione S-tranferase P1 by Western blot analysis. Our results clearly showed that caloric restriction significantly improves the plasmatic oxidative/inflammatory balance in parallel with a major increase in circulating adiponectin levels. Additionally, at the level of adipose tissue, we found a positive modulation of both anti-inflammatory and antioxidant pathways. These adaptations, induced by caloric restriction, with the achievement of normal weight, suggest that inflammatory and redox imbalance in obese aged rats appear to be more linked to obesity than to aging. Full article
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18 pages, 2054 KiB  
Article
Identification of Toxicity Parameters Associated with Combustion Produced Soot Surface Chemistry and Particle Structure by in Vitro Assays
by Heba Al Housseiny, Madhu Singh, Shaneeka Emile, Marvin Nicoleau, Randy L. Vander Wal and Patricia Silveyra
Biomedicines 2020, 8(9), 345; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8090345 - 11 Sep 2020
Cited by 10 | Viewed by 2929
Abstract
Air pollution has become the world’s single biggest environmental health risk of the past decade, causing millions of yearly deaths worldwide. One of the dominant air pollutants is fine particulate matter (PM2.5), which is a product of combustion. Exposure to PM [...] Read more.
Air pollution has become the world’s single biggest environmental health risk of the past decade, causing millions of yearly deaths worldwide. One of the dominant air pollutants is fine particulate matter (PM2.5), which is a product of combustion. Exposure to PM2.5 has been associated with decreased lung function, impaired immunity, and exacerbations of lung disease. Accumulating evidence suggests that many of the adverse health effects of PM2.5 exposure are associated with lung inflammation and oxidative stress. While the physical structure and surface chemistry of PM2.5 are surrogate measures of particle oxidative potential, little is known about their contributions to negative health effects. In this study, we used functionalized carbon black particles as surrogates for atmospherically aged combustion-formed soot to assess the effects of PM2.5 surface chemistry in lung cells. We exposed the BEAS-2B lung epithelial cell line to different soot at a range of concentrations and assessed cell viability, inflammation, and oxidative stress. Our results indicate that exposure to soot with varying particle surface composition results in differential cell viability rates, the expression of pro-inflammatory and oxidative stress genes, and protein carbonylation. We conclude that particle surface chemistry, specifically oxygen content, in soot modulates lung cell inflammatory and oxidative stress responses. Full article
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22 pages, 4936 KiB  
Article
Inflammation in Dry Eye Syndrome: Identification and Targeting of Oxylipin-Mediated Mechanisms
by Dmitry V. Chistyakov, Olga S. Gancharova, Viktoriia E. Baksheeva, Veronika V. Tiulina, Sergei V. Goriainov, Nadezhda V. Azbukina, Marina S. Tsarkova, Andrey A. Zamyatnin, Jr., Pavel P. Philippov, Marina G. Sergeeva, Ivan I. Senin and Evgeni Yu. Zernii
Biomedicines 2020, 8(9), 344; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8090344 - 11 Sep 2020
Cited by 10 | Viewed by 5786
Abstract
Dry eye syndrome (DES) is characterized by decreased tear production and stability, leading to desiccating stress, inflammation and corneal damage. DES treatment may involve targeting the contributing inflammatory pathways mediated by polyunsaturated fatty acids and their derivatives, oxylipins. Here, using an animal model [...] Read more.
Dry eye syndrome (DES) is characterized by decreased tear production and stability, leading to desiccating stress, inflammation and corneal damage. DES treatment may involve targeting the contributing inflammatory pathways mediated by polyunsaturated fatty acids and their derivatives, oxylipins. Here, using an animal model of general anesthesia-induced DES, we addressed these pathways by characterizing inflammatory changes in tear lipidome, in correlation with pathophysiological and biochemical signs of the disease. The decline in tear production was associated with the infiltration of inflammatory cells in the corneal stroma, which manifested one to three days after anesthesia, accompanied by changes in tear antioxidants and cytokines, resulting in persistent damage to the corneal epithelium. The inflammatory response manifested in the tear fluid as a short-term increase in linoleic and alpha-linolenic acid-derived oxylipins, followed by elevation in arachidonic acid and its derivatives, leukotriene B4 (5-lipoxigenase product), 12-hydroxyeicosatetraenoic acid (12-lipoxigeanse product) and prostaglandins, D2, E2 and F2α (cyclooxygenase products) that was observed for up to 7 days. Given these data, DES was treated by a novel ophthalmic formulation containing a dimethyl sulfoxide-based solution of zileuton, an inhibitor of 5-lipoxigenase and arachidonic acid release. The therapy markedly improved the corneal state in DES by attenuating cytokine- and oxylipin-mediated inflammatory responses, without affecting tear production rates. Interestingly, the high efficacy of the proposed therapy resulted from the synergetic action of its components, namely, the general healing activity of dimethyl sulfoxide, suppressing prostaglandins and the more specific effect of zileuton, downregulating leukotriene B4 (inhibition of T-cell recruitment), as well as upregulating docosahexaenoic acid (activation of resolution pathways). Full article
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13 pages, 1349 KiB  
Article
Gender-Related Differences in Trimethylamine and Oxidative Blood Biomarkers in Cardiovascular Disease Patients
by Laura Bordoni, Donatella Fedeli, Marco Piangerelli, Iwona Pelikant-Malecka, Adrianna Radulska, Joanna J. Samulak, Angelika K. Sawicka, Lukasz Lewicki, Leszek Kalinowski, Robert A. Olek and Rosita Gabbianelli
Biomedicines 2020, 8(8), 238; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8080238 - 23 Jul 2020
Cited by 6 | Viewed by 2407
Abstract
Gender differences in the burden of cardiovascular disease (CVD) have been observed worldwide. In this study, plasmatic levels of trimethylamine (TMA) and blood oxidative biomarkers have been evaluated in 358 men (89 controls and 269 CVD patients) and 189 women (64 control and [...] Read more.
Gender differences in the burden of cardiovascular disease (CVD) have been observed worldwide. In this study, plasmatic levels of trimethylamine (TMA) and blood oxidative biomarkers have been evaluated in 358 men (89 controls and 269 CVD patients) and 189 women (64 control and 125 CVD patients). The fluorescence technique was applied to determine erythrocyte membrane fluidity using 1,6-diphenyl-1,3,5-hexatriene (DPH) and Laurdan, while lipid hydroperoxides were assessed by diphenyl−1-pyrenylphosphine (DPPP). Results show that levels of plasmatic TMA were higher in healthy men with respect to healthy women (p = 0.0001). Significantly lower TMA was observed in male CVD patients (0.609 ± 0.104 μM) compared to healthy male controls (0.680 ± 0.118 μM) (p < 0.001), while higher levels of TMA were measured in female CVD patients (0.595 ± 0.115 μM) with respect to female controls (0.529 ± 0.073 μM) (p < 0.001). DPPP was significantly higher in healthy control men than in women (p < 0.001). Male CVD patients displayed a lower value of DPPP (2777 ± 1924) compared to healthy controls (5528 ± 2222) (p < 0.001), while no significant changes were measured in females with or without CVD (p > 0.05). Membrane fluidity was significantly higher (p < 0.001) in the hydrophobic bilayer only in control male subjects. In conclusion, gender differences were observed in blood oxidative biomarkers, and DPPP value might be suggested as a biomarker predictive of CVD only in men. Full article
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17 pages, 5137 KiB  
Article
Effects of an 8-Week Protein Supplementation Regimen with Hyperimmunized Cow Milk on Exercise-Induced Organ Damage and Inflammation in Male Runners: A Randomized, Placebo Controlled, Cross-Over Study
by Sihui Ma, Takaki Tominaga, Kazue Kanda, Kaoru Sugama, Chiaki Omae, Shunsuke Hashimoto, Katsuhiko Aoyama, Yasunobu Yoshikai and Katsuhiko Suzuki
Biomedicines 2020, 8(3), 51; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8030051 - 04 Mar 2020
Cited by 12 | Viewed by 4778
Abstract
Prolonged strenuous exercise may induce inflammation, cause changes in gastrointestinal permeability, and lead to other unfavorable biological changes and diseases. Nutritional approaches have been used to prevent exercise-induced inflammatory responses and gastrointestinal disorders. Hyperimmunized milk, obtained by immunizing cows against specific antigens, promotes [...] Read more.
Prolonged strenuous exercise may induce inflammation, cause changes in gastrointestinal permeability, and lead to other unfavorable biological changes and diseases. Nutritional approaches have been used to prevent exercise-induced inflammatory responses and gastrointestinal disorders. Hyperimmunized milk, obtained by immunizing cows against specific antigens, promotes the development of immunity against pathogens, promotes anti-inflammatory effects, and protects intestinal function. Immune protein (IMP) is a concentrated product of hyperimmunized milk and is a more promising means of supplementation to protect against acute infections and inflammation. To determine whether IMP has protective properties against exercise-induced gastrointestinal dysfunction and inflammation, we examined biochemical markers, intestinal damage markers, and pro-/anti-inflammatory profiles of young male runners using a randomized, placebo controlled, cross-over design. Urine samples were collected and used for measurements of creatinine, N-acetyl-β-d-glucosaminidase, osmotic pressure, and specific gravity. Titin was measured as a muscle damage marker. Further, urine concentrations of complement 5a, calprotectin, fractalkine, myeloperoxidase, macrophage colony-stimulating factor, monocyte chemotactic protein-1, intestinal fatty acid binding protein (I-FABP), interferon (IFN)-γ, interleukin (IL)-1β, IL-1 receptor antagonist, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12p40, and tumor necrosis factor (TNF)-α were measured by enzyme-linked immunosorbent assays. We demonstrated that urine osmotic pressure, urine specific gravity, I-FABP, IFN-γ, IL-1β, and TNF-α were reduced by 8 weeks of IMP supplementation, indicating that IMP may have potential in preventing strenuous exercise-induced renal dysfunction, increased intestinal permeability, and inflammation. Thus, IMP supplementation may be a feasible nutritional approach for the prevention of unfavorable exercise-induced symptoms. Full article
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14 pages, 2439 KiB  
Article
The Use of Natural Agents to Counteract Telomere Shortening: Effects of a Multi-Component Extract of Astragalus mongholicus Bunge and Danazol
by Isabelle Guinobert, Claude Blondeau, Bruno Colicchio, Noufissa Oudrhiri, Alain Dieterlen, Eric Jeandidier, Georges Deschenes, Valérie Bardot, César Cotte, Isabelle Ripoche, Patrice Carde, Lucile Berthomier and Radhia M’Kacher
Biomedicines 2020, 8(2), 31; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8020031 - 12 Feb 2020
Cited by 6 | Viewed by 5730
Abstract
A link between telomere shortening and oxidative stress was found in aging people and patients with cancer or inflammatory diseases. Extracts of Astragalus spp. are known to stimulate telomerase activity, thereby compensating telomere shortening. We characterized a multi-component hydroethanolic root extract (HRE) of [...] Read more.
A link between telomere shortening and oxidative stress was found in aging people and patients with cancer or inflammatory diseases. Extracts of Astragalus spp. are known to stimulate telomerase activity, thereby compensating telomere shortening. We characterized a multi-component hydroethanolic root extract (HRE) of Astragalus mongholicus Bunge and assessed its effects on telomeres compared to those of danazol. Astragalosides I to IV, flavonoids, amino acids and sugars were detected in the HRE. Samples of peripheral blood lymphocytes with short telomeres from 18 healthy donors (mean age 63.5 years; range 32–86 years) were exposed to a single dose of 1 µg/mL HRE or danazol for three days. Telomere length and telomerase expression were then measured. Significant elongation of telomeres associated to a less toxicity was observed in lymphocytes from 13/18 donors following HRE treatment (0.54 kb (0.15–2.06 kb)) and in those from 9/18 donors after danazol treatment (0.95 kb (0.06–2.06 kb)). The rate of cells with short telomeres (<3 kb) decreased in lymphocytes from all donors after exposure to either HRE or danazol, telomere elongation being telomerase-dependent. These findings suggest that the HRE could be used for the management of age-related diseases. Full article
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9 pages, 1438 KiB  
Article
Anti-Inflammatory Effects of Diospyrin on Lipopolysaccharide-Induced Inflammation Using RAW 264.7 Mouse Macrophages
by Adnan Shahidullah, Ji-Young Lee, Young-Jin Kim, Syed Muhammad Ashhad Halimi, Abdur Rauf, Hyun-Ju Kim, Bong-Youn Kim and Wansu Park
Biomedicines 2020, 8(1), 11; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8010011 - 11 Jan 2020
Cited by 6 | Viewed by 4809
Abstract
Diospyrin is a bisnaphthoquinonoid medicinal compound derived from Diospyros lotus, with known anti-cancer, anti-tubercular, and anti-leishmanial activities against Leishmania donovani. However, the effects of diospyrin on lipopolysaccharide (LPS)-induced macrophage activation and inflammation are not fully reported. In this study, the anti-inflammatory [...] Read more.
Diospyrin is a bisnaphthoquinonoid medicinal compound derived from Diospyros lotus, with known anti-cancer, anti-tubercular, and anti-leishmanial activities against Leishmania donovani. However, the effects of diospyrin on lipopolysaccharide (LPS)-induced macrophage activation and inflammation are not fully reported. In this study, the anti-inflammatory effects of diospyrin on LPS-induced macrophages were examined. Diospyrin showed no toxicity in RAW 264.7 at concentrations of up to 10 μM. Diospyrin moderated the production of nitric oxide (NO), monocyte chemotactic protein-1, macrophage inflammatory protein-1β, interleukin (IL)-6, IL-10, granulocyte colony-stimulating factor, granulocyte macrophage colony-stimulating factor, vascular endothelial growth factor, leukemia inhibitory factor, and RANTES/CCL5, as well as calcium release in LPS-induced RAW 264.7, at concentrations of up to 10 μM significantly (p < 0.05). Diospyrin also significantly inhibited the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and mRNA expression of C/EBP homologous protein (CHOP), as well as tumor necrosis factor receptor superfamily member 6 (Fas), in LPS-induced RAW 264.7 cells at concentrations of up to 10 μM (p < 0.05). Diospyrin exhibits anti-inflammatory properties mediated via inhibition of NO, and cytokines in LPS-induced mouse macrophages via the ER-stressed calcium-p38 MAPK/CHOP/Fas pathway. Full article
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Review

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15 pages, 547 KiB  
Review
Implications of Breast Cancer Chemotherapy-Induced Inflammation on the Gut, Liver, and Central Nervous System
by Taurean Brown, DeLawrence Sykes and Antiño R. Allen
Biomedicines 2021, 9(2), 189; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9020189 - 13 Feb 2021
Cited by 22 | Viewed by 6311
Abstract
Breast Cancer is still one of the most common cancers today; however, with advancements in diagnostic and treatment methods, the mortality and survivorship of patients continues to decrease and increase, respectively. Commonly used treatments today consist of drug combinations, such as doxorubicin and [...] Read more.
Breast Cancer is still one of the most common cancers today; however, with advancements in diagnostic and treatment methods, the mortality and survivorship of patients continues to decrease and increase, respectively. Commonly used treatments today consist of drug combinations, such as doxorubicin and cyclophosphamide; docetaxel, doxorubicin, and cyclophosphamide; or doxorubicin, cyclophosphamide, and paclitaxel. Although these combinations are effective at destroying cancer cells, there is still much to be understood about the effects that chemotherapy can have on normal organ systems such as the nervous system, gastrointestinal tract, and the liver. Patients can experience symptoms of cognitive impairments or “chemobrain”, such as difficulty in concentrating, memory recollection, and processing speed. They may also experience gastrointestinal (GI) distress symptoms such as diarrhea and vomiting, as well as hepatotoxicity and long term liver damage. Chemotherapy treatment has also been shown to induce peripheral neuropathy resulting in numbing, pain, and tingling sensations in the extremities of patients. Interestingly, researchers have discovered that this array of symptoms that cancer patients experience are interconnected and mediated by the inflammatory response. Full article
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20 pages, 1661 KiB  
Review
Can Exercise-Induced Muscle Damage Be a Good Model for the Investigation of the Anti-Inflammatory Properties of Diet in Humans?
by Spyridon Methenitis, Ioanna Stergiou, Smaragdi Antonopoulou and Tzortzis Nomikos
Biomedicines 2021, 9(1), 36; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines9010036 - 05 Jan 2021
Cited by 12 | Viewed by 4149
Abstract
Subclinical, low-grade, inflammation is one of the main pathophysiological mechanisms underlying the majority of chronic and non-communicable diseases. Several methodological approaches have been applied for the assessment of the anti-inflammatory properties of nutrition, however, their impact in human body remains uncertain, because of [...] Read more.
Subclinical, low-grade, inflammation is one of the main pathophysiological mechanisms underlying the majority of chronic and non-communicable diseases. Several methodological approaches have been applied for the assessment of the anti-inflammatory properties of nutrition, however, their impact in human body remains uncertain, because of the fact that the majority of the studies reporting anti-inflammatory effect of dietary patterns, have been performed under laboratory settings and/or in animal models. Thus, the extrapolation of these results to humans is risky. It is therefore obvious that the development of an inflammatory model in humans, by which we could induce inflammatory responses to humans in a regulated, specific, and non-harmful way, could greatly facilitate the estimation of the anti-inflammatory properties of diet in a more physiological way and mechanistically relevant way. We believe that exercise-induced muscle damage (EIMD) could serve as such a model, either in studies investigating the homeostatic responses of individuals under inflammatory stimuli or for the estimation of the anti-inflammatory or pro-inflammatory potential of dietary patterns, foods, supplements, nutrients, or phytochemicals. Thus, in this review we discuss the possibility of exercise-induced muscle damage being an inflammation model suitable for the assessment of the anti-inflammatory properties of diet in humans. Full article
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14 pages, 637 KiB  
Review
Therapeutic Potential of Porcine Liver Decomposition Product: New Insights and Perspectives for Microglia-Mediated Neuroinflammation in Neurodegenerative Diseases
by Tamotsu Tsukahara, Hisao Haniu, Takeshi Uemura and Yoshikazu Matsuda
Biomedicines 2020, 8(11), 446; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8110446 - 22 Oct 2020
Cited by 12 | Viewed by 3095
Abstract
It is widely accepted that microglia-mediated inflammation contributes to the progression of neurodegenerative diseases; however, the precise mechanisms through which these cells contribute remain to be elucidated. Microglia, as the primary immune effector cells of the brain, play key roles in maintaining central [...] Read more.
It is widely accepted that microglia-mediated inflammation contributes to the progression of neurodegenerative diseases; however, the precise mechanisms through which these cells contribute remain to be elucidated. Microglia, as the primary immune effector cells of the brain, play key roles in maintaining central nervous system (CNS) homeostasis. Microglia are located throughout the brain and spinal cord and may account for up to 15% of all cells in the brain. Activated microglia express pro-inflammatory cytokines that act on the surrounding brain and spinal cord. Microglia may also play a detrimental effect on nerve cells when they gain a chronic inflammatory function and promote neuropathologies. A key feature of microglia is its rapid morphological change upon activation, characterized by the retraction of numerous fine processes and the gradual acquisition of amoeba-like shapes. These morphological changes are also accompanied by the expression and secretion of inflammatory molecules, including cytokines, chemokines, and lipid mediators that promote systemic inflammation during neurodegeneration. This may be considered a protective response intended to limit further injury and initiate repair processes. We previously reported that porcine liver decomposition product (PLDP) induces a significant increase in the Hasegawa’s Dementia Scale-Revised (HDS-R) score and the Wechsler Memory Scale (WMS) in a randomized, double-blind, placebo-controlled study in healthy humans. In addition, the oral administration of porcine liver decomposition product enhanced visual memory and delayed recall in healthy adults. We believe that PLDP is a functional food that aids cognitive function. In this review, we provide a critical assessment of recent reports of lysophospholipids derived from PLDP, a rich source of phospholipids. We also highlight some recent findings regarding bidirectional interactions between lysophospholipids and microglia and age-related neurodegenerative diseases such as dementia and Alzheimer’s disease. Full article
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18 pages, 1712 KiB  
Review
The Anti-Inflammatory and Antioxidant Properties of n-3 PUFAs: Their Role in Cardiovascular Protection
by Francesca Oppedisano, Roberta Macrì, Micaela Gliozzi, Vincenzo Musolino, Cristina Carresi, Jessica Maiuolo, Francesca Bosco, Saverio Nucera, Maria Caterina Zito, Lorenza Guarnieri, Federica Scarano, Caterina Nicita, Anna Rita Coppoletta, Stefano Ruga, Miriam Scicchitano, Rocco Mollace, Ernesto Palma and Vincenzo Mollace
Biomedicines 2020, 8(9), 306; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8090306 - 25 Aug 2020
Cited by 129 | Viewed by 10062
Abstract
Polyunsaturated fatty acids (n-3 PUFAs) are long-chain polyunsaturated fatty acids with 18, 20 or 22 carbon atoms, which have been found able to counteract cardiovascular diseases. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in particular, have been found to produce both vaso- and [...] Read more.
Polyunsaturated fatty acids (n-3 PUFAs) are long-chain polyunsaturated fatty acids with 18, 20 or 22 carbon atoms, which have been found able to counteract cardiovascular diseases. Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in particular, have been found to produce both vaso- and cardio-protective response via modulation of membrane phospholipids thereby improving cardiac mitochondrial functions and energy production. However, antioxidant properties of n-3 PUFAs, along with their anti-inflammatory effect in both blood vessels and cardiac cells, seem to exert beneficial effects in cardiovascular impairment. In fact, dietary supplementation with n-3 PUFAs has been demonstrated to reduce oxidative stress-related mitochondrial dysfunction and endothelial cell apoptosis, an effect occurring via an increased activity of endogenous antioxidant enzymes. On the other hand, n-3 PUFAs have been shown to counteract the release of pro-inflammatory cytokines in both vascular tissues and in the myocardium, thereby restoring vascular reactivity and myocardial performance. Here we summarize the molecular mechanisms underlying the anti-oxidant and anti-inflammatory effect of n-3 PUFAs in vascular and cardiac tissues and their implication in the prevention and treatment of cardiovascular disease. Full article
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14 pages, 838 KiB  
Review
Relationship between Diet, Microbiota, and Healthy Aging
by Elisa Sanchez-Morate, Lucia Gimeno-Mallench, Kristine Stromsnes, Jorge Sanz-Ros, Aurora Román-Domínguez, Sergi Parejo-Pedrajas, Marta Inglés, Gloria Olaso, Juan Gambini and Cristina Mas-Bargues
Biomedicines 2020, 8(8), 287; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8080287 - 14 Aug 2020
Cited by 22 | Viewed by 5697
Abstract
Due to medical advances and lifestyle changes, population life expectancy has increased. For this reason, it is important to achieve healthy aging by reducing the risk factors causing damage and pathologies associated with age. Through nutrition, one of the pillars of health, we [...] Read more.
Due to medical advances and lifestyle changes, population life expectancy has increased. For this reason, it is important to achieve healthy aging by reducing the risk factors causing damage and pathologies associated with age. Through nutrition, one of the pillars of health, we are able to modify these factors through modulation of the intestinal microbiota. The Mediterranean and Oriental diets are proof of this, as well as the components present in them, such as fiber and polyphenols. These generate beneficial effects on the body thanks, in part, to their interaction with intestinal bacteria. Likewise, the low consumption of products with high fat content favors the state of the microbiota, contributing to the maintenance of good health. Full article
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18 pages, 1651 KiB  
Review
Antiplatelet Therapy for Acute Respiratory Distress Syndrome
by Chuan-Mu Chen, Hsiao-Ching Lu, Yu-Tang Tung and Wei Chen
Biomedicines 2020, 8(7), 230; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8070230 - 21 Jul 2020
Cited by 20 | Viewed by 12679
Abstract
Acute respiratory distress syndrome (ARDS) is a common and devastating syndrome that contributes to serious morbidities and mortality in critically ill patients. No known pharmacologic therapy is beneficial in the treatment of ARDS, and the only effective management is through a protective lung [...] Read more.
Acute respiratory distress syndrome (ARDS) is a common and devastating syndrome that contributes to serious morbidities and mortality in critically ill patients. No known pharmacologic therapy is beneficial in the treatment of ARDS, and the only effective management is through a protective lung strategy. Platelets play a crucial role in the pathogenesis of ARDS, and antiplatelet therapy may be a potential medication for ARDS. In this review, we introduce the overall pathogenesis of ARDS, and then focus on platelet-related mechanisms underlying the development of ARDS, including platelet adhesion to the injured vessel wall, platelet-leukocyte-endothelium interactions, platelet-related lipid mediators, and neutrophil extracellular traps. We further summarize antiplatelet therapy, including aspirin, glycoprotein IIb/IIIa receptor antagonists, and P2Y12 inhibitors for ARDS in experimental and clinical studies and a meta-analysis. Novel aspirin-derived agents, aspirin-triggered lipoxin, and aspirin-triggered resolvin D1 are also described here. In this narrative review, we summarize the current knowledge of the role of platelets in the pathogenesis of ARDS, and the potential benefits of antiplatelet therapy for the prevention and treatment of ARDS. Full article
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14 pages, 596 KiB  
Review
Targeting Redox Imbalance as an Approach for Diabetic Kidney Disease
by Keiichiro Matoba, Yusuke Takeda, Yosuke Nagai, Tamotsu Yokota, Kazunori Utsunomiya and Rimei Nishimura
Biomedicines 2020, 8(2), 40; https://0-doi-org.brum.beds.ac.uk/10.3390/biomedicines8020040 - 22 Feb 2020
Cited by 30 | Viewed by 4164
Abstract
Diabetic kidney disease (DKD) is a worldwide public health problem. It is the leading cause of end-stage renal disease and is associated with increased mortality from cardiovascular complications. The tight interactions between redox imbalance and the development of DKD are becoming increasingly evident. [...] Read more.
Diabetic kidney disease (DKD) is a worldwide public health problem. It is the leading cause of end-stage renal disease and is associated with increased mortality from cardiovascular complications. The tight interactions between redox imbalance and the development of DKD are becoming increasingly evident. Numerous cascades, including the polyol and hexosamine pathways have been implicated in the oxidative stress of diabetes patients. However, the precise molecular mechanism by which oxidative stress affects the progression of DKD remains to be elucidated. Given the limited therapeutic options for DKD, it is essential to understand how oxidants and antioxidants are controlled in diabetes and how oxidative stress impacts the progression of renal damage. This review aims to provide an overview of the current status of knowledge regarding the pathological roles of oxidative stress in DKD. Finally, we summarize recent therapeutic approaches to preventing DKD with a focus on the anti-oxidative effects of newly developed anti-hyperglycemic agents. Full article
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