Oxidative Stress In Animal Models Research Articles

The effect of acupuncture on oxidative stress in animal models of vascular dementia: a systematic review and meta-analysis

BackgroundGrowing evidence showed that acupuncture may improve cognitive function by reducing oxidative stress, key to the pathogenesis in vascular dementia (VaD), but this is yet to be systematically analysed. This study aimed to summarize and evaluate the effect of acupuncture on oxidative stress in animal models of VaD.MethodEight databases including PubMed, Embase, Web of Science, Cochrane library, CNKI, Wan Fang, CBM, and VIP were searched since their establishment until April 2023, for studies that reported the effect of acupuncture on oxidative stress in VaD animal models. Relevant literature was screened, and information was extracted by two reviewers. The primary outcomes were the levels of oxidative stress indicators. The methodological quality was assessed via the SYRCLE Risk of Bias Tool. Statistical analyses were performed using the RevMan and Stata software.ResultsIn total, 22 studies with 747 animals were included. The methodology of most studies had flaws or uncertainties. The meta-analysis indicated that, overall, acupuncture significantly reduced the expression of pro-oxidants including reactive oxygen species (standardized mean differences [SMDs] = -4.29, 95% confidence interval [CI]: -6.26, -2.31), malondialdehyde (SMD = -2.27, 95% CI: -3.07, -1.47), nitric oxide (SMD = -0.85, 95% CI: -1.50, -0.20), and nitric oxide synthase (SMD = -1.01, 95% CI: -1.69, -0.34) and enhanced the levels of anti-oxidants including super oxide dismutase (SMD = 2.80, 95% CI: 1.98, 3.61), glutathione peroxidase (SMD = 1.32, 95% CI: -0.11, 2.76), and catalase (SMD = 1.31, 95% CI: 0.05, 2.58) in VaD animal models. In subgroup analyses, acupuncture showed significant effects on most variables. Only partial modelling methods and treatment duration could interpret the heterogeneity of some outcomes.ConclusionAcupuncture may inhibit oxidative stress to improve cognitive deficits in animal models of VaD. Nevertheless, the methodological quality is unsatisfactory. More high-quality research with a rigorous design and further experimental researches and clinical trials are needed to confirm these findings.Systematic review registrationThis study was registered in PROSPERO (CRD42023411720).

Ginkgo Biloba and Long COVID: In Vivo and In Vitro Models for the Evaluation of Nanotherapeutic Efficacy.

Coronavirus infections are neuroinvasive and can provoke injury to the central nervous system (CNS) and long-term illness consequences. They may be associated with inflammatory processes due to cellular oxidative stress and an imbalanced antioxidant system. The ability of phytochemicals with antioxidant and anti-inflammatory activities, such as Ginkgo biloba, to alleviate neurological complications and brain tissue damage has attracted strong ongoing interest in the neurotherapeutic management of long COVID. Ginkgo biloba leaf extract (EGb) contains several bioactive ingredients, e.g., bilobalide, quercetin, ginkgolides A-C, kaempferol, isorhamnetin, and luteolin. They have various pharmacological and medicinal effects, including memory and cognitive improvement. Ginkgo biloba, through its anti-apoptotic, antioxidant, and anti-inflammatory activities, impacts cognitive function and other illness conditions like those in long COVID. While preclinical research on the antioxidant therapies for neuroprotection has shown promising results, clinical translation remains slow due to several challenges (e.g., low drug bioavailability, limited half-life, instability, restricted delivery to target tissues, and poor antioxidant capacity). This review emphasizes the advantages of nanotherapies using nanoparticle drug delivery approaches to overcome these challenges. Various experimental techniques shed light on the molecular mechanisms underlying the oxidative stress response in the nervous system and help comprehend the pathophysiology of the neurological sequelae of SARS-CoV-2 infection. To develop novel therapeutic agents and drug delivery systems, several methods for mimicking oxidative stress conditions have been used (e.g., lipid peroxidation products, mitochondrial respiratory chain inhibitors, and models of ischemic brain damage). We hypothesize the beneficial effects of EGb in the neurotherapeutic management of long-term COVID-19 symptoms, evaluated using either in vitro cellular or in vivo animal models of oxidative stress.

The Water Extract of Ampelopsis grossedentata Alleviates Oxidative Stress and Intestinal Inflammation.

Oxidative stress is recognized as a significant contributor to the development and progression of inflammation and disruptions in the balance of gut microflora, commonly referred to as intestinal dysbiosis. It is crucial that safe and effective antioxidant and anti-inflammatory agents are identified to address these conditions. Ampelopsis grossedentata, a natural plant abundant in flavonoids and primarily found in southern China, has demonstrated potent antioxidant properties. However, the extent to which flavonoids in A. grossedentata impact intestinal inflammation and alter the composition of the gut microbiome remains to be fully understood. The purpose of this study was to explore the potential benefits of using A. grossedentata as an antioxidant and anti-inflammatory agent in the context of intestinal inflammation, both in vitro and in vivo. We first conducted an initial comparison of the effects of dihydromyricetin (DMY), an alcohol extract of A. grossedentata (AEA, 82% total flavonoids), and a water extract of A. grossedentata (WEA, 57% total flavonoids) on the cell viability and intestinal barrier integrity of porcine epithelial cells IPEC-J2. Although the total flavonoid content is much lower in WEA than in AEA, the results show that they have similar effects. Subsequently, the antioxidant properties of WEA were compared with those of commonly utilized antioxidants in vitro. Lastly, the antioxidant and anti-inflammatory properties of WEA, as well as its impacts on gut microbiota, were evaluated in animal models, including mice and Drosophila. In summary, the results of our study indicate that WEA, due to its antioxidant properties, exhibits a protective effect on the intestinal barrier function in porcine epithelial cell line IPEC-J2. Additionally, WEA demonstrates a positive correlation with DPPH, ABTS radical scavenging rate, FRAP, and reducing power under in vitro settings. Furthermore, WEA was shown to effectively alleviate oxidative stress in animal models by reducing the levels of pro-inflammatory cytokines and increasing the antioxidant enzyme activity in the liver, as well as by activating the Nrf2 signaling pathway in the duodenum. Additionally, WEA was able to regulate gut microbiota, promoting the growth of beneficial bacteria and inhibiting harmful microbes, as well as extending the lifespan of Drosophila. Overall, these findings suggest that WEA may serve as a valuable dietary supplement for addressing oxidative stress and inflammation through its anti-inflammatory and prebiotic effects, which are conferred via the Nrf2/Keap1 pathway.

Effect of melatonin on oxidative stress indicators in animal models of fibrosis: A systematic review and meta-analysis.

Imbalance of oxidative stress has been detected in a range of fibrotic diseases. Melatonin as an indoleamine hormone plays an important role in regulating the circadian rhythm of human, while in recent years, its antioxidant effect has also attracted increasing attention. This study aimed to perform a systematic review and meta-analysis to comprehensively evaluate the antioxidant effect of melatonin in animal models of fibrosis. The PubMed, Cochrane Library, EMBASE, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang database, China Science and Technology Journal Database (VIP), and SinoMed databases were searched from inception to March 1st, 2022 to retrieve eligible studies that evaluated the effect of melatonin supplementation on the levels of malondialdehyde (MDA), lipid peroxidation (LPO), nitric oxide (NO), superoxide dismutase (SOD), glutathione (GSH), glutathione peroxidase (GPx), and catalase (CAT) in animal models of fibrosis. A total of 64 studies were included in this meta-analysis. The results showed that melatonin supplementation significantly reduced the levels of oxidative indicators including MDA (P<0.00001), LPO (P<0.00001) and NO (P<0.0001), and elevated the levels of antioxidant indicators including GSH (P<0.00001), GPx (P<0.00001) and SOD (P<0.00001) in fibrotic diseases. Our research findings showed that melatonin supplementation could significantly reduce the levels of oxidative indicators including MDA, LPO and NO and elevate the levels of antioxidant indicators including GSH, GPx and SOD so as to correct oxidative stress in animal models of fibrosis. However, no significant changes were observed in CAT level. More clinical studies are needed to further confirm the beneficial role of melatonin in fibrotic diseases.

A systematic review of the effect of photobiomodulation on the neuroinflammatory response in animal models of neurodegenerative diseases.

This systematic review examines the effect of photobiomodulation (PBM), the application of red to near infrared light on body tissues, on the neuroinflammatory response and oxidative stress in animal models of neurodegenerative diseases. The research question and search protocol were prospectively registered on the PROSPERO database. Neurodegenerative diseases are becoming evermore prevalent in the ageing populations across theWestern world, with no disease-modifying or neuroprotective treatment options being available. Hence there is a real need for the development of effective treatment options for patients. Inflammatory responses and oxidative stress within the central nervous system have a strong correlation with neuronal cell death. PBM is a non-invasive therapeutic option that has shown efficacy and promising effects inanimal models of neurodegenerative disease; many studies have reported neuroprotection and improved behavioural outcomes. To the best of our knowledge, therehas been no previous study that has reviewed theanti-inflammatory and the antioxidant effect of PBM inthe context of neurodegeneration. This review has examined this relationship in animal models of a range ofneurodegenerative diseases. We found that PBM can effectively reduce glial activation, pro-inflammatory cytokine expression and oxidative stress, whilst increasing anti-inflammatory glial responses and cytokines, and antioxidant capacity. These positive outcomes accompanied the neuroprotection evident after PBM treatment. Our review provides further indication that PBM can be developed intoan effective non-pharmacological intervention for neurodegenerative diseases.

The effect of acupuncture on oxidative stress: A systematic review and meta-analysis of animal models.

Oxidative stress is involved in the occurrence and development of multiple diseases. Acupuncture shows an excellent clinical efficacy in practical application but its mechanism remains unclear. This systematic review and meta-analysis was aimed at assessing the effect of acupuncture on oxidative stress in animal models. PubMed, Embase, and Web of Science database were retrieved for randomized controlled trials about acupuncture on oxidative stress in animal models from inception to August 2021. Two reviewers independently screened and extracted articles according to inclusion and exclusion criteria. We used the mean difference (MD)/standardized mean difference (SMD) to perform an effect size analysis and selected fixed-effect or random-effect models to pool the data, depending on a 95% confidence interval (CI). A total of 12 studies comprising 125 samples were included in the quantitative meta-analysis. Compared with sham acupuncture, acupuncture (manual acupuncture, electropuncture, and laser acupuncture) reduced the level of malondialdehyde (SMD, -3.03; CI, -4.40, -1.65; p < 0.00001) and increased the levels of superoxide dismutase (SMD, 3.39; CI, 1.99, 4.79; p < 0.00001), glutathione peroxidase (SMD, 2.21; CI, 1.10, 3.32; p < 0.00001), and catalase (SMD, 2.80; CI, 0.57, 5.03; p = 0.01). This meta-analysis indicated that acupuncture can regulate oxidative stress by lowering the lipid peroxidation and activating the antioxidant enzyme system. In consideration of heterogeneity between studies, future studies should be performed by complying with strict standards and increasing sample size in animal experiments to reduce bias.

Potential Utility of Natural Products against Oxidative Stress in Animal Models of Multiple Sclerosis

Multiple sclerosis (MS) is an autoimmune-mediated degenerative disease of the central nervous system (CNS) characterized by immune cell infiltration, demyelination and axonal injury. Oxidative stress-induced inflammatory response, especially the destructive effect of immune cell-derived free radicals on neurons and oligodendrocytes, is crucial in the onset and progression of MS. Therefore, targeting oxidative stress-related processes may be a promising preventive and therapeutic strategy for MS. Animal models, especially rodent models, can be used to explore the in vivo molecular mechanisms of MS considering their similarity to the pathological processes and clinical signs of MS in humans and the significant oxidative damage observed within their CNS. Consequently, these models have been used widely in pre-clinical studies of oxidative stress in MS. To date, many natural products have been shown to exert antioxidant effects to attenuate the CNS damage in animal models of MS. This review summarized several common rodent models of MS and their association with oxidative stress. In addition, this review provides a comprehensive and concise overview of previously reported natural antioxidant products in inhibiting the progression of MS.

Evaluation of betulinic acid effects on pain, memory, anxiety, catalepsy, and oxidative stress in animal model of Parkinson's disease.

Parkinson's disease (PD) is known for motor impairments. Betulinic acid (BA) is a natural compound with antioxidant activity. The present study addresses the question of whether BA affects motor and non-motor dysfunctions and molecular changes in the rat model of PD. The right medial forebrain bundle was lesioned by injection of 6-hydroxydopamine in Male Wistar rats (10-12weeks old, 270-320g). Animals were divided into Sham, PD, 3 treated groups with BA (0.5, 5, and 10mg/kg, IP), and a positive control group received L-dopa (20mg/kg, P.O) for 7days. rigidity, anxiety, analgesia, and memory were assessed by bar test, open-field, elevated plus-maze (EPM), tail-flick, and shuttle box. Additionally, the malondialdehyde (MDA), Superoxide dismutase (SOD), glutathione peroxidase (GPx) activity, Brain-derived neurotrophic factor (BDNF) and Interleukin 10 (IL10) levels in the whole brain were measured. BA significantly reversed the 6-hydroxydopamine-induced motor and memory complication in the bar test and shuttle box. It modified anxiety-like behavior neither in open-field nor in EPM. It only decreased the time spent in open arms. Moreover, no significant changes were found in the tail-flick between treatment and sham groups. On the other hand, the level of MDA & IL10 were decreased, while the activity of GPx levels of SOD & BDNF in the rats' brains was increased. Our results showed that BA as a free radical scavenger can account for a possible promise as a good therapeutic agent for motor and non-motor complications in PD however further studies may be needed.

Propolis Mitigates Rifampicin/Isoniazid-induced Lipid-redox and Metabolic Profile in an Experimental Animal Model of Oxidative Stress

Objective: Adverse drug reactions are the most common cause of drug withdrawal in chronic treatment settings. Tuberculosis (TB) has been considered a recurrent and relapsing disease that needs long-term therapy. Most patients suffer from the adverse effects of TB therapy. Hence, various remedies were used to tackle these adverse effects including antioxidant vitamins, herbal remedies, and others. Aims: The present intervention study aims to investigate the role of propolis in protecting the animal model against oxidant/antioxidant induced by TB therapy together with the propolis role in modulation of metabolic profile as part of lipid peroxidation context. Methods: Serum was collected from rats exposed to rifampicin/isoniazid with or without propolis therapy alongside the control placebo group for comparison. Results: The results have shown a significant (p&lt;0.05) reduction of malondialdehyde and significant (p&lt;0.05) elevation of total antioxidant status. Lipid profile positively improved indicated by significantly reduced total cholesterol, triglyceride, and elevated high-density lipoprotein. Conclusion: our study confirmed that propolis provides protection against redox and metabolic derangement induced by rifampicin/isoniazid medications which are in current TB therapy, therefore, we do advise the use of propolis as an adjunct therapy for patients on such medications.

Investigation of efficacy of asenapine on passive avoidance learning and memory and oxidative stress in animal model of seizure-induced with pentylenetetrazole

Asenapine (ASE) has been used for treatment of bipolar disorder. There is also evidence that it may be useful in the treatment of neurodegenerative disorders. In this regard, the efficacy of ASE in an experimental model of seizure and memory impairment caused by seizures in rats has been investigated in the present study. Seizures in male Wistar rats (200-250 g) were induced by pentylenetetrazole (PTZ, 60 mg/kg, intraperitoneally (i.p.)), and the anticonvulsant effect of ASE (0.5 and 1 mg/kg, i.p.) was evaluated. The effect on memory was assessed using passive avoidance (PA) test in a shuttle box apparatus. After behavioral tests, the animals underwent deep anesthesia and were euthanized painlessly. Serum was isolated for oxidative stress assays (nitric oxide (NO), and glutathione (GSH)). Intraperitoneal injection of ASE decreased the mean number of myoclonic jerks and duration of generalized tonic clonic seizures (GTCS) and increased the mean latency of myoclonic jerk and GTCS compared to the PTZ group. Moreover, in the PA test, ASE caused a significant increase in retention latency (RL) and total time spent in the light compartment (TLC) compared to the PTZ group. Biochemical tests showed that ASE was able to significantly increase GSH serum levels and significantly reduce NO serum levels compared to the PTZ group. Overall, this study suggests the potential neuroprotective effects of ASE in a model of memory impairment caused by seizures via the mechanism of inhibition of the oxidative stress pathway.

Investigation of efficacy of asenapine on passive avoidance learning and memory and oxidative stress in animal model of seizure-induced with pentylenetetrazole

Asenapine (ASE) has been used for treatment of bipolar disorder. There is also evidence that it may be useful in the treatment of neurodegenerative disorders. In this regard, the efficacy of ASE in an experimental model of seizure and memory impairment caused by seizures in rats has been investigated in the present study. Seizures in male Wistar rats (200-250 g) were induced by pentylenetetrazole (PTZ, 60 mg/kg, intraperitoneally (i.p.)), and the anticonvulsant effect of ASE (0.5 and 1 mg/kg, i.p.) was evaluated. The effect on memory was assessed using passive avoidance (PA) test in a shuttle box apparatus. After behavioral tests, the animals underwent deep anesthesia and were euthanized painlessly. Serum was isolated for oxidative stress assays (nitric oxide (NO), and glutathione (GSH)). Intraperitoneal injection of ASE decreased the mean number of myoclonic jerks and duration of generalized tonic clonic seizures (GTCS) and increased the mean latency of myoclonic jerk and GTCS compared to the PTZ group. Moreover, in the PA test, ASE caused a significant increase in retention latency (RL) and total time spent in the light compartment (TLC) compared to the PTZ group. Biochemical tests showed that ASE was able to significantly increase GSH serum levels and significantly reduce NO serum levels compared to the PTZ group. Overall, this study suggests the potential neuroprotective effects of ASE in a model of memory impairment caused by seizures via the mechanism of inhibition of the oxidative stress pathway.

Probing the antioxidant potential of Juglans regia (walnut) against arthritis-induced oxidative stress in Sprague Dawley rats.

Oxidative stress is the underlying cause of various chronic diseases and can contribute to its progression. Plant-based therapeutics are effective in the prevention of various chronic diseases through the management of underlying causes. Walnuts owing to their rich phytochemistry possess antioxidative potential. In this context, the present research was designed to explore the therapeutic potential of walnut against arthritis-induced oxidative stress in rat model. Purposely, 50 Sprague Dawley rats were separated into five groups of 10 rats each. The rats were categorized as G0 (negative control), G1 (positive control), G2 (methotrexate), G3 (walnut feed), and G4 (walnut extract). Walnut feed and extract significantly reduced oxidative stress by improving the antioxidant enzymes in arthritic rats. Total oxidative stress was reduced by 41.44% and 21.52% in G3 while 52.81% and 36.76% in G4 when compared with G1 and G2 , respectively. Antioxidant enzyme levels in serum were significantly improved after the walnut-based interventions. Evidently, superoxide dismutase level improved by 74.5% in G3 and 83.40% in G4 , while catalase level increased by 51.99% in G3 and 61.34% in G4 , respectively, when compared with G1 . Liver function biomarkers, that is, ALP and AST, were decreased in G3 and G4 when compared with G1 and G2 . The histopathological examination illustrated the promising role of walnut-based interventions in conserving the structural integrity of hepatic and renal tissues. Meanwhile, gene expression analysis revealed that walnut treatments protected from oxidative damage by the downregulation of Dual-oxidases expression. Conclusively, walnut feed and extract might serve as potent antioxidant intervention with no potential side effects. PRACTICAL APPLICATIONS: The present work was aimed to evaluate the efficacy of walnut-based interventions against arthritis-induced oxidative stress. The walnut-based interventions positively modulated the antioxidant enzymes, liver, and kidney functions, while downregulating the gene associated with oxidative stress in animal model. Consequently, the current findings suggest wider applications of walnuts to avoid free radical induced damage during arthritis; however, human intervention studies may be carried out to further understand the mechanism of their bioefficacy.

Comparison of three methods for in vivo quantification of glutathione in tissues of hypertensive rats

Glutathione (γ-L-glutamyl-L-cysteinyl-glycine, GSH) is a tripeptide that is part of the antioxidant defense system and contributes to numerous redox-regulatory processes. In vivo, reduced GSH and oxidized glutathione disulfide (GSSG) are present in redox equilibrium and their ratio provides important information on the cellular redox state. Here, we compared three different methods for in vivo quantification of glutathione in tissues of hypertensive rats, an accepted animal model of oxidative stress. In the present study, we used hypertensive rats (infusion of 1 mg/kg/d angiotensin-II for 7 days) to determine the levels of reduced GSH and/or GSH/GSSG ratios in different tissue samples. We used an HPLC-based method with direct electrochemical detection (HPLC/ECD) and compared it with Ellman’s reagent (DTNB) dependent derivatization of reduced GSH to the GS-NTB adduct and free NTB (UV/Vis HPLC) as well as with a commercial GSH/GSSG assay (Oxiselect). Whereas all three methods indicated overall a decreased redox state in hypertensive rats, the assays based on HPLC/ECD and DTNB derivatization provided the most significant differences. We applied a direct, fast and sensitive method for electrochemical GSH detection in tissues from hypertensive animals, and confirmed its reliability for in vivo measurements by head-to-head comparison with two other established assays. The HPLC/ECD but not DTNB and Oxiselect assays yielded quantitative GSH data but all three assays reflected nicely the qualitative redox changes and functional impairment in hypertensive rats. However, especially our GSH/GSSG values are lower than reported by others pointing to problems in the work-up protocol.

Lifelong soya consumption in males does not increase lifespan but increases health span under a metabolic stress such as type 2 diabetes mellitus

Soya consumption can decrease oxidative stress in animal models. Moreover, phytoestrogens such as genistein, present in soya, can mimic some of the beneficial effects of estrogens and are devoid of significant side effects, such as cancer. In this study, we have performed a controlled lifelong study with male OF1 mice that consumed either a soya-free diet or a soya-rich diet. We show that, although we found an increase in the expression and activity of antioxidant enzymes in soya-consuming mice, it did not increase lifespan. We reasoned that the soya diet could not increase lifespan in a very healthy population, but perhaps it could extend health span in stressed animals such as type 2 diabetic Goto Kakizaki (GK) rats. Indeed, this was the case: we found that male GK rats consuming a soya-rich diet developed the disease at a lower rate and, therefore, lived longer than soya-free diet-consuming rats.

The Use of Natural Compounds as a Strategy to Counteract Oxidative Stress in Animal Models of Diabetes Mellitus.

Diabetes mellitus (DM) is a chronic metabolic disease characterised by insulin deficiency, resulting in hyperglycaemia, a characteristic symptom of type 2 diabetes mellitus (DM2). DM substantially affects numerous metabolic pathways, resulting in β-cell dysfunction, insulin resistance, abnormal blood glucose levels, impaired lipid metabolism, inflammatory processes, and excessive oxidative stress. Oxidative stress can affect the body’s normal physiological function and cause numerous cellular and molecular changes, such as mitochondrial dysfunction. Animal models are useful for exploring the cellular and molecular mechanisms of DM and improving novel therapeutics for their safe use in human beings. Due to their health benefits, there is significant interest in a wide range of natural compounds that can act as naturally occurring anti-diabetic compounds. Due to rodent models’ relatively similar physiology to humans and ease of handling and housing, they are widely used as pre-clinical models for studying several metabolic disorders. In this review, we analyse the currently available rodent animal models of DM and their advantages and disadvantages and highlight the potential anti-oxidative effects of natural compounds and their mechanisms of action.

Effects of vanillic acid on Aβ1-40-induced oxidative stress and learning and memory deficit in male rats

Alzheimer's disease (AD) is a neurodegenerative disease, in which the accumulation of β-amyloid (Aβ) peptide in the extracellular space causes a progressive reduction in cognitive performance. Aβ stimulates active oxygen species generation leading to oxidative stress and neural cell death. Vanillic Acid (VA) is the oxidant form of vanillin widely found in vanilla beans. VA has many properties, such as suppressing apoptosis and eliminating the harmful effects of oxidative stress in animal models. The VA effects on impaired learning and memory in Aβ rats were assessed. Forty adults male Wistar rats were assigned to the following five groups in random: the control, sham (received saline (vehicle) via intracerebroventricular (ICV) injection), Aβ (received Aβ1–40 via ICV injection), VA (50 mg/kg by oral gavage once a day through four weeks), and Aβ + VA (50 mg/kg) groups. Open field test, novel object recognition (NOR) test, Morris water maze (MWM) test, and passive avoidance learning (PAL) task were performed, and finally, we determined the malondialdehyde (MDA), total antioxidant capacity (TAC) and total oxidant status (TOS) levels. Aβ decreased the cognitive memory in NOR, spatial memory in MWM, and passive avoidance memory in PAL tests. In contrast, VA improved learning and memory in the treated group. Aβ significantly increased MDA and TOS and decreased TAC levels, whereas VA treatment significantly reversed TAC, TOS and MDA levels. In conclusion, VA decreased the Aβ effects on learning and memory by suppressing oxidative stress and can be regarded as a neuroprotective substance in AD.

Dietary Modulation of Oxidative Stress From Edible Insects: A Mini-Review.

Edible insects are proposed as a nutritious and environmentally sustainable alternative source to animal proteins, due to their numerous advantages in terms of reduced ecological impact and high nutritional value. However, the novelty for edible insects relies on the content of bioactive ingredients potentially able to induce a functional effect in the body. The present review summarizes the main findings on the antioxidant properties of edible insects available in the literature. A total of 30 studies involving animals, cell cultures, or in vitro experimental studies evaluating the antioxidant effect of edible insects are presented in this work. When the antioxidant activity was investigated, using a wide variety of in vitro tests and in cellular models, positive results were shown. Dietary supplementation with edible insects was also able to counteract dietary oxidative stress in animal models, restoring the balance of antioxidant enzymes and reducing the formation of oxidation damage markers. On the basis of the reviewed evidences, edible insects might represent a source of novel redox ingredients at low ecological impact able to modulate oxidative stress. However, due to the fact that majority of these evidences have been obtained in vitro and in cellular and animal models, dietary intervention trials are needed to assess the efficacy of edible insect consumption to modulate redox status in humans.

Characterization of oxidative stress in animal model of neonatal hypoxia.

ABSTRACTPurposeTo evaluate the oxidative stress in swine neonates submitted to hypoxia.MethodsTen large white piglets, healthy newborns, of both sexes, were divided into two groups and submitted to an experimental hypoxia protocol with reduced inspired oxygen fraction. The hypoxia group, composed of six animals, was submitted to oxygen reduction for 180 min. The animals in the control group, n = 4, were handled and evaluated simultaneously, but without oxygen reduction.Results180 min after the start of the hypoxic insult, a significant difference was observed in the oximetry, and heart rate of the hypoxia group was compared to the control group (p<0.05). There was no significant difference in the oxidative stress analyses. Reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (TBARS), protein carbonyl (PC), and myeloperoxidase (MPO) in the piglets’ brain tissue were analyzed.ConclusionsHypoxia causes adverse effects in swine neonates, although there is a natural physiological resistance of swine neonates to respond to this insult. Analyses of GSH, SOD, CAT, TBARS, MPO, and PC were tabulated and are presented as parameters for further studies to be carried out on an animal model of swine hypoxia.

Oxidative Stress and Microglial Response in Retinitis Pigmentosa.

An imbalance between the production of reactive oxygen species (ROS) and anti-oxidant capacity results in oxidative injury to cellular components and molecules, which in turn disturbs the homeostasis of cells and organs. Although retinitis pigmentosa (RP) is a hereditary disease, non-genetic biological factors including oxidative stress also modulate or contribute to the disease progression. In animal models of RP, the degenerating retina exhibits marked oxidative damage in the nucleic acids, proteins, and lipids, and anti-oxidant treatments substantially suppress photoreceptor cell death and microgliosis. Although the mechanisms by which oxidative stress mediates retinal degeneration have not been fully elucidated, our group has shown that oxidative DNA damage and its defense system are key regulators of microglial activation and photoreceptor degeneration in RP. In this review, we summarize the current evidence regarding oxidative stress in animal models and patients with RP. The clinical efficacy of anti-oxidant treatments for RP has not been fully established. Nevertheless, elucidating key biological processes that underlie oxidative damage in RP will be pivotal to understanding the pathology and developing a potent anti-oxidant strategy that targets specific cell types or molecules under oxidative stress.

Role of CAPE in reducing oxidative stress in animal models with traumatic brain injury

IntroductionThe central nervous system (CNS) is the most metabolically active organ characterized by high oxygen demand and relatively low anti-oxidative activity, which makes neurons and glia highly susceptible to damage by reactive oxygen and nitrogen byproducts as well as neurodegeneration. Free radicals are associated with secondary injuries that occur after a primary brain injury. Some of these free radical products include F2-Isoprostane (F2-IsoPs), malondialdehyde (MDA), 4-hydroxy-2-nonenal (4-HNE) and acrolein. MethodsIn this study we measured serum F2-IsoPs levels as markers of free radical activity in 10–12 week-old male Sprague-Dawley rats weighing 200–300 g, all rats (n = 10) subjected with a head injury according to the modified marmourou model, then divided into 2 groups, one group treated with CAPE (Caffeic Acid Phenethyl Ester) (n = 5) and the other not treated with CAPE (n = 5), serum levels in the two groups were compared starting from day-0 (before brain injury), day-4 and day-7. ResultsWe found lower F2-IsoPs levels in the group that received the CAPE treatment compared to the group that did not receive the CAPE treatment. ConclusionCAPE is capable of significantly reducing oxidative stress in brain injury.