scholarly journals Small Molecule Oligopeptides Isolated from Walnut (Juglans regia L.) and Their Anti-Fatigue Effects in Mice

Molecules ◽  
2018 ◽  
Vol 24 (1) ◽  
pp. 45 ◽  
Author(s):  
Rui Liu ◽  
Lan Wu ◽  
Qian Du ◽  
Jin-Wei Ren ◽  
Qi-He Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Small Molecule ◽  
Mitochondrial Function ◽  
Biological Activities ◽  
Juglans Regia ◽  
Glycogen Storage ◽  
Vehicle Group ◽  
Positive Effects ◽  
Metabolism Enzymes

Walnut (Juglans regia L.) is unique for its extensive biological activities and pharmaceutical properties. There are few studies on walnut oligopeptides (WOPs), which are small molecule peptides extracted from walnuts. This study aimed to evaluate the anti-fatigue effects of WOPs on ICR mice and explore the possible underlying mechanism. Mice were randomly divided into four experimental sets and each set of mice were then randomly divided into four groups. The vehicle group was administered distilled water, and the three WOP intervention groups were orally administered WOP solution at a dose of 110, 220, and 440 mg/kg of body weight, respectively. After 30 days of WOP intervention, the anti-fatigue activity of WOPs were evaluated using the weight-loaded swimming test and by measuring the change of biochemical parameters, glycogen storage and energy metabolism enzymes, anti-oxidative capacity and mitochondrial function. It was observed that WOPs could significantly prolong the swimming time, decrease the accumulation of lactate dehydrogenase (LDH), creatine kinase (CK), blood urea nitrogen (BUN) and blood lactic acid (BLA), and increased the glycogen storage of liver and gastrocnemius muscle. WOPs also markedly inhibited fatigue induced oxidative stress by increasing the activity of superoxide dismutase (SOD), glutathione peroxidase (GPX) and decreasing the content malondialdehyde (MDA). Notably, WOPs improved the activity of pyruvate kinase (PK), succinate dehydrogenase (SDH), Na+-K+-ATPase, and enhanced the mRNA expression of mitochondrial biogenesis factors and mitochondrial DNA content in skeletal muscles of mice. These results suggest that WOPs have beneficial anti-fatigue effects, which may be attributed to their positive effects on increasing glycogen storage, improving energy metabolism, inhibiting oxidative stress, enhancing mitochondrial function in skeletal muscle, and ameliorating the cell damage and the muscular injury.

scholarly journals Alterations in Energy Metabolism, Mitochondrial Function and Redox Homeostasis in GK Diabetic Rat Tissues Treated with Aspirin

Life ◽  
2022 ◽  
Vol 12 (1) ◽  
pp. 104
Author(s):  
Annie John ◽  
Layla Amiri ◽  
Jasmin Shafarin ◽  
Saeed Tariq ◽  
Ernest Adeghate ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Mitochondrial Function ◽  
Redox Homeostasis ◽  
Diabetic Rats ◽  
Endocrine Function ◽  
Diabetic Rat ◽  
Rat Tissues ◽  
Gk Rats ◽  
And Oxidative Stress

Our recent studies have demonstrated that aspirin treatment prevents inflammatory and oxidative stress-induced alterations in mitochondrial function, improves glucose tolerance and pancreatic endocrine function and preserves tissue-specific glutathione (GSH)-dependent redox homeostasis in Goto-Kakizaki (GK) diabetic rats. In the current study, we have investigated the mechanism of action of aspirin in maintaining mitochondrial bioenergetics and redox metabolism in the liver and kidneys of GK rats. Aspirin reduced the production of reactive oxygen species (ROS) and oxidative stress-induced changes in GSH metabolism. Aspirin treatment also improved mitochondrial respiratory function and energy metabolism, in addition to regulating the expression of cell signaling proteins that were altered in diabetic animals. Ultrastructural electron microscopy studies revealed decreased accumulation of glycogen in the liver of aspirin-treated diabetic rats. Hypertrophic podocytes with irregular fusion of foot processes in the renal glomerulus and detached microvilli, condensed nuclei and degenerated mitochondria observed in the proximal convoluted tubules of GK rats were partially restored by aspirin. These results provide additional evidence to support our previous observation of moderation of diabetic complications by aspirin treatment in GK rats and may have implications for cautious use of aspirin in the therapeutic management of diabetes.

scholarly journals T58. EFFECTIVENESS OF ORALLY ADMINISTERED CO-ENZYME Q10 FOR SCHIZOPHRENIA: COGNITIVE, FUNCTIONAL AND BIOCHEMICAL OUTCOMES FROM A DOUBLE BLIND, RANDOMISED, PLACEBO CONTROLLED TRIAL

2020 ◽  
Vol 46 (Supplement_1) ◽  
pp. S253-S253
Author(s):  
April Hargreaves ◽  
Aine Maguire ◽  
Christina Mooney ◽  
Iain Hargreaves ◽  
Robert Heaton ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Schizoaffective Disorder ◽  
Controlled Study ◽  
Protective Agent ◽  
Double Blind ◽  
Positive Effects ◽  
Coq10 Supplementation

Abstract Background Coenzyme Q10 (CoQ10) is an endogenous compound that is essential for energy production within the mitochondria and also functions as a potent anti-oxidant, inhibiting oxidative stress and damage. Often deficits in CoQ10 are associated with fatigue, and cognitive and psychological impairment. In light of its many functions, CoQ10 supplementation to minimise decline and improve symptoms has been investigated in multiple disorders including neurological and neuropsychiatric disorders, with results indicating positive effects on fatigue, cognitive impairment and affective difficulties for disorders such as bipolar disorder and chronic fatigue syndrome. There is also evidence of mitochondrial dysfunction in schizophrenia. In light of this evidence, the current study aimed to investigate the potential effect of CoQ10 supplementation on 1) cognitive function and 2) psychological and physical health in schizophrenia and schizoaffective disorder. Methods A double blind, randomised, placebo controlled study was conducted to assess the effects of CoQ10 supplementation (300mg/day) on cognitive, psychological and physical variables in 70 patients with schizophrenia and schizoaffective disorder. The effects of CoQ10 supplementation were compared to placebo at 3 and 6 months. Plasma CoQ10 was measured at all time points, along with measures of mitochondrial function (via plasma lactate concentration). Sensitivity analysis followed an intention to treat approach that used multiple imputations to account for missing values. Results Overall there was no effect of CoQ10 supplementation on cognitive outcome measures. This is despite observing an increase in plasma CoQ10 concentration in the CoQ10 group compared to the placebo. CoQ10 supplementation also had no effect on mitochondrial function, energy, psychological symptoms, quality of life, functional status, physical activity or blood pressure at either time point. Discussion There is considerable evidence that mitochondrial dysfunction is present in patients with schizophrenia and schizoaffective disorder, and this dysfunction is implicated in the manifestation of cognitive impairment and clinical symptoms. CoQ10 can be taken as a nutritional supplement with minimal side effects to target mitochondrial dysfunction via promoting ATP generation and increasing antioxidant capacity. However, we found no effect of CoQ10 supplementation on any variable under investigation. It is possible that CoQ10 might act as a protective agent against exacerbated oxidative stress in these patients, and future studies might be warranted to examine this possibility. However, the current data is conclusive that CoQ10 supplementation does not ameliorate existing deficits in schizophrenia. These findings are translatable to clinical and community settings.

scholarly journals Mitochondrial function and energy metabolism in neuronal HT22 cells resistant to oxidative stress

2014 ◽  
Vol 171 (8) ◽  
pp. 2147-2158 ◽  
Author(s):  
Annika Pfeiffer ◽  
Martin Jaeckel ◽  
Jan Lewerenz ◽  
Rebecca Noack ◽  
Alireza Pouya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Mitochondrial Function ◽  
Ht22 Cells

scholarly journals Decreased in vitro Mitochondrial Function is Associated with Enhanced Brain Metabolism, Blood Flow, and Memory in Surfl-Deficient Mice

2013 ◽  
Vol 33 (10) ◽  
pp. 1605-1611 ◽  
Author(s):  
Ai-Ling Lin ◽  
Daniel A Pulliam ◽  
Sathyaseelan S Deepa ◽  
Jonathan J Halloran ◽  
Stacy A Hussong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Mitochondrial Function ◽  
Cognitive Aging ◽  
Brain Function ◽  
Brain Metabolism ◽  
Functional Changes ◽  
Positive Effects ◽  
Age Related

Recent studies have challenged the prevailing view that reduced mitochondrial function and increased oxidative stress are correlated with reduced longevity. Mice carrying a homozygous knockout (KO) of the Surf1 gene showed a significant decrease in mitochondrial electron transport chain Complex IV activity, yet displayed increased lifespan and reduced brain damage after excitotoxic insults. In the present study, we examined brain metabolism, brain hemodynamics, and memory of Surf1 KO mice using in vitro measures of mitochondrial function, in vivo neuroimaging, and behavioral testing. We show that decreased respiration and increased generation of hydrogen peroxide in isolated Surf1 KO brain mitochondria are associated with increased brain glucose metabolism, cerebral blood flow, and lactate levels, and with enhanced memory in Surf1 KO mice. These metabolic and functional changes in Surf1 KO brains were accompanied by higher levels of hypoxia-inducible factor 1 alpha, and by increases in the activated form of cyclic AMP response element-binding factor, which is integral to memory formation. These findings suggest that Surf1 deficiency-induced metabolic alterations may have positive effects on brain function. Exploring the relationship between mitochondrial activity, oxidative stress, and brain function will enhance our understanding of cognitive aging and of age-related neurologic disorders.

scholarly journals Icaritin Provides Neuroprotection in Parkinson’s Disease by Attenuating Neuroinflammation, Oxidative Stress, and Energy Deficiency

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 529
Author(s):  
Hao Wu ◽  
Xi Liu ◽  
Ze-Yu Gao ◽  
Ming Lin ◽  
Xin Zhao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Energy Metabolism ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Nlrp3 Inflammasome ◽  
Neuronal Damage ◽  
Ionization Mass ◽  
Voltage Dependent Anion Channel

Neuroinflammation, oxidative stress, and mitochondrial dysfunction are all important pathogenic mechanisms underlying motor dysfunction and dopaminergic neuronal damage observed in patients with Parkinson’s disease (PD). However, despite extensive efforts, targeting inflammation and oxidative stress using various approaches has not led to meaningful clinical outcomes, and mitochondrial enhancers have also failed to convincingly achieve disease-modifying effects. We tested our hypothesis that treatment approaches in PD should simultaneously reduce neuroinflammation, oxidative stress, and improve alterations in neuronal energy metabolism using the flavonoid icaritin in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Using matrix-assisted laser desorption/ionization–mass spectrometry imaging (MALDI-MSI), coupled with biochemical analyses and behavioral tests, we demonstrate that icaritin improves PD by attenuating the the NOD-like receptor family pyrin domain-containing protein 3 (NLRP3) inflammasome activity and stabilizing mitochondrial function, based on our extensive analyses showing the inhibition of NLRP3 inflammasome, reduction of NLRP3-mediated IL-1β secretion, and improvements in the levels of antioxidant molecules. Our data also indicated that icaritin stabilized the levels of proteins related to mitochondrial function, such as voltage-dependent anion channel (VDAC) and ATP synthase subunit beta (ATP5B), as well as those of molecules related to energy metabolism, such as ATP and ADP, ultimately improving mitochondrial dysfunction. By employing molecular docking, we also discovered that icaritin can interact with NLRP3, VDAC, ATP5B, and several blood–brain barrier (BBB)-related proteins. These data provide insights into the promising therapeutic potential of icaritin in PD.

Metabolomics of Healthy Berry Fruits

2019 ◽  
Vol 25 (37) ◽  
pp. 4888-4902 ◽  
Author(s):  
Gilda D'Urso ◽  
Sonia Piacente ◽  
Cosimo Pizza ◽  
Paola Montoro
Keyword(s):  
Biological Activities ◽  
Biologically Active ◽  
In Vivo Studies ◽  
Bioactive Metabolites ◽  
Active Metabolites ◽  
Positive Effects ◽  
Cell Functions ◽  
Berry Fruits

The consumption of berry-type fruits has become very popular in recent years because of their positive effects on human health. Berries are in fact widely known for their health-promoting benefits, including prevention of chronic disease, cardiovascular disease and cancer. Berries are a rich source of bioactive metabolites, such as vitamins, minerals, and phenolic compounds, mainly anthocyanins. Numerous in vitro and in vivo studies recognized the health effects of berries and their function as bioactive modulators of various cell functions associated with oxidative stress. Plants have one of the largest metabolome databases, with over 1200 papers on plant metabolomics published only in the last decade. Mass spectrometry (MS) and NMR (Nuclear Magnetic Resonance) are the most important analytical technologies on which the emerging ''omics'' approaches are based. They may provide detection and quantization of thousands of biologically active metabolites from a tissue, working in a ''global'' or ''targeted'' manner, down to ultra-trace levels. In the present review, we highlighted the use of MS and NMR-based strategies and Multivariate Data Analysis for the valorization of berries known for their biological activities, important as food and often used in the preparation of nutraceutical formulations.

Adenosine Receptor Modulation of Hypoxic-ischemic Injury in Striatum of Newborn Piglets

2020 ◽  
Vol 17 (4) ◽  
pp. 510-517
Author(s):  
Santiago Ortega-Gutierrez ◽  
Brandy Jones ◽  
Alan Mendez-Ruiz ◽  
Pankhil Shah ◽  
Michel T. Torbey
Keyword(s):  
Oxidative Stress ◽  
Atpase Activity ◽  
Neuronal Injury ◽  
Receptor Activation ◽  
Adult Mortality ◽  
Vehicle Group ◽  
Sodium Potassium ◽  
Receptor Modulation ◽  
A2a Receptor ◽  
Potassium Atpase

Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of pediatric and adult mortality and morbidity. Unfortunately, to date, no effective treatment has been identified. In the striatum, neuronal injury is analogous to the cellular mechanism of necrosis observed during NMethyl- D-Aspartate (NMDA) excitotoxicity. Adenosine acts as a neuromodulator in the central nervous system, the role of which relies mostly on controlling excitatory glutamatergic synapses. Objective: To examine the effect of pretreatment of SCH58261, an adenosine 2A (A2A) receptor antagonist and modulator of NMDA receptor function, following hypoxic-ischemia (HI) on sodium- potassium ATPase (Na+, K+-ATPase) activity and oxidative stress. Methods: Piglets (4-7 days old) were subjected to 30 min hypoxia and 7 min of airway occlusion producing asphyxic cardiac arrest. Groups were divided into four categories: HI samples were divided into HI-vehicle group (n = 5) and HI-A2A group (n = 5). Sham controls were divided into Sham vehicle (n = 5) and Sham A2A (n = 5) groups. Vehicle groups were pretreated with 0.9% saline, whereas A2A animals were pretreated with SCH58261 10 min prior to intervention. Striatum samples were collected 3 h post-arrest. Sodium-potassium ATPase (Na+, K+-ATPase) activity, malondialdehyde (MDA) + 4-hydroxyalkenals (4-HDA) and glutathione (GSH) levels were compared. Results: Pretreatment with SCH58261 significantly attenuated the decrease in Na+, K+-ATPase, decreased MDA+4-HDA levels and increased GSH in the HI-A2A group when compared to HIvehicle. Conclusion: A2A receptor activation may contribute to neuronal injury in newborn striatum after HI in association with decreased Na+, K+-ATPase activity and increased oxidative stress.

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