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Antioxidants (Basel, Switzerland) Jul 2023Epilepsy is a neurological disorder characterized by epileptic seizures resulting from neuronal hyperexcitability, which may be related to failures in Na,K-ATPase... (Review)
Review
Antioxidant Therapy Reduces Oxidative Stress, Restores Na,K-ATPase Function and Induces Neuroprotection in Rodent Models of Seizure and Epilepsy: A Systematic Review and Meta-Analysis.
Epilepsy is a neurological disorder characterized by epileptic seizures resulting from neuronal hyperexcitability, which may be related to failures in Na,K-ATPase activity and oxidative stress participation. We conducted this study to investigate the impact of antioxidant therapy on oxidative stress, Na,K-ATPase activity, seizure factors, and mortality in rodent seizure/epilepsy models induced by pentylenetetrazol (PTZ), pilocarpine (PILO), and kainic acid (KA). After screening 561 records in the MEDLINE, EMBASE, Web of Science, Science Direct, and Scopus databases, 22 were included in the systematic review following the PRISMA guidelines. The meta-analysis included 14 studies and showed that in epileptic animals there was an increase in the oxidizing agents nitric oxide (NO) and malondialdehyde (MDA), with a reduction in endogenous antioxidants reduced glutathione (GSH) and superoxide dismutase (SO). The Na,K-ATPase activity was reduced in all areas evaluated. Antioxidant therapy reversed all of these parameters altered by seizure or epilepsy induction. In addition, there was a percentage decrease in the number of seizures and mortality, and a meta-analysis showed a longer seizure latency in animals using antioxidant therapy. Thus, this study suggests that the use of antioxidants promotes neuroprotective effects and mitigates the effects of epilepsy. The protocol was registered in the Prospective Register of Systematic Reviews (PROSPERO) CRD42022356960.
PubMed: 37507936
DOI: 10.3390/antiox12071397 -
Phytotherapy Research : PTR Sep 2023To determine the pharmaceutical applications, we assessed the evidence from preclinical studies about the hypoglycemic, hypolipidemic, and antioxidant potential of... (Meta-Analysis)
Meta-Analysis Review
To determine the pharmaceutical applications, we assessed the evidence from preclinical studies about the hypoglycemic, hypolipidemic, and antioxidant potential of Pistacia atlantica (PA) as a natural source for prevention and treatment of diabetes. A comprehensive literature search of the articles published until March 12, 2022 was conducted on PubMed, Embase, Web of Sciences, and Scopus databases, using relevant keywords. This meta-analysis included 12 articles that examined the blood glucose (BG), insulin, homeostatic model assessment for insulin resistance (HOMA-IR), triglyceride (TG), total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), malondialdehyde (MDA) and superoxide dismutase (SOD). A random-effects model was used to estimate the pooled effect size. Findings indicated that PA supplementation significantly decreased BG, HOMA-IR, TC, TG, and MDA, and increased insulin and SOD in diabetic animals compared with control group (p < .05). However, PA supplementation had no significant effects on HDL-C (p > .05). The subgroup analysis also confirmed the beneficial effect of PA supplementation with longer duration (>4 weeks) and higher doses (≥100 mg/kg/day) as well as in the extract type. The studies have heterogeneity associated with methodological diversity and there were some concerns about the risk of bias, especially about randomization and blind outcome assessment. This meta-analysis provided convincing evidence for antidiabetic, hypolipidemic, and antioxidant activity of PA in animals. Further high-quality studies are needed to firmly establish the clinical efficacy of the plant.
Topics: Animals; Antioxidants; Hypoglycemic Agents; Pistacia; Plant Extracts; Diabetes Mellitus; Blood Glucose; Insulin; Insulin Resistance; Superoxide Dismutase; Triglycerides; Cholesterol
PubMed: 37428094
DOI: 10.1002/ptr.7898 -
The Cochrane Database of Systematic... Oct 2023Free oxygen radicals have been implicated in the pathogenesis of bronchopulmonary dysplasia (BPD) in preterm infants. Superoxide dismutase (SOD) is a naturally occurring... (Review)
Review
BACKGROUND
Free oxygen radicals have been implicated in the pathogenesis of bronchopulmonary dysplasia (BPD) in preterm infants. Superoxide dismutase (SOD) is a naturally occurring enzyme which provides a defense against such oxidant injury. Providing supplementary SOD has been tested in clinical trials to prevent BPD in preterm infants.
OBJECTIVES
To determine the efficacy and safety of SOD in the prevention and treatment of BPD on mortality and other complications of prematurity in infants at risk for, or having BPD.
SEARCH METHODS
We searched CENTRAL, PubMed, Embase, and three trials registers on 22 September 2022 together with reference checking, citation searching and contact with study authors to identify additional studies.
SELECTION CRITERIA
Randomized, quasi-randomized and cluster-randomized controlled trials (RCTs) where the participants were preterm infants who had developed, or were at risk of developing BPD, and who were randomly allocated to receive either SOD (in any form, by any route, any dose, anytime) or placebo, or no treatment.
DATA COLLECTION AND ANALYSIS
We used standard Cochrane methods. Our primary outcomes were BPD defined as an oxygen requirement at 28 days, BPD defined as oxygen at 36 weeks' postmenstrual age, neonatal mortality, mortality prior to discharge, and BPD or death at 36 weeks' postmenstrual age. We reported risk ratio (RR) and risk difference (RD) with 95% confidence intervals (CIs) for the dichotomous outcomes. We used GRADE to assess certainty of evidence for each outcome.
MAIN RESULTS
We included three RCTs (380 infants) on SOD administration in preterm infants at risk for BPD, and no studies in preterm infants with evolving BPD / early respiratory insufficiency. The evidence is very uncertain about the effect of SOD on BPD defined as an oxygen requirement at 28 days (RR 1.09, 95% CI 0.94 to 1.26; RD 0.06, 95% CI -0.05 to 0.16, 1 study, 302 infants; I for RR and RD not applicable), BPD defined as oxygen at 36 weeks' postmenstrual age (RR 0.96, 95% CI 0.72 to 1.29; RD -0.01, 95% CI -0.11 to 0.09, 2 studies, 335 infants; I for RR and RD = 0%), neonatal mortality (RR 0.98, 95% CI 0.57 to 1.68; RD -0.00, 95% CI -0.08 to 0.07, 2 studies, 335 infants; I for RR and RD = 0%), and mortality prior to discharge (RR 1.20, 95% CI 0.53 to 2.71; RD 0.04, 95% CI -0.14 to 0.23, 2 studies, 78 infants; I for RR and RD = 0%). No studies reported BPD or death at 36 weeks' postmenstrual age. The evidence is very uncertain about the effect of SOD on retinopathy of prematurity any stage (RR 0.95, 95% CI 0.78 to 1.15; RD -0.03, 95% CI -0.15 to 0.08, 2 studies, 335 infants; Ifor RR = 0%, I for RD = 8%), and severe retinopathy of prematurity (ROP) (RR 0.97, 95% CI 0.57 to 1.65; RD -0.01, 95% CI -0.10 to 0.09, 1 study, 244 infants; I for RR and RD not applicable). No studies reported moderate to severe neurodevelopmental outcome at 18 to 24 months. Certainty of evidence was very low for all outcomes. We identified no ongoing trials.
AUTHORS' CONCLUSIONS
The evidence is very uncertain about the effect of SOD on BPD defined as an oxygen requirement at 28 days, BPD defined as oxygen at 36 weeks' postmenstrual age, neonatal mortality and mortality prior to discharge compared to placebo. No studies reported BPD or death at 36 weeks' postmenstrual age and need for supplemental oxygen. The evidence is very uncertain about the effect of SOD on retinopathy of prematurity any stage and severe retinopathy of prematurity. No studies reported moderate to severe neurodevelopmental outcome at 18 to 24 months. The effects of SOD in preterm infants has not been reported in any trial in the last few decades, considering that the most recent trial on SOD in preterm infants was conducted in 1997/1998, and no new studies are ongoing. In the light of the limited available evidence, new data from preclinical and observational studies are needed to justify the conduction of new RCTs. Observational studies might report how SOD is administered, including indication, dose and association with relevant outcomes such as mortality, BPD and long-term neurodevelopment.
Topics: Infant, Newborn; Infant; Humans; Retinopathy of Prematurity; Bronchopulmonary Dysplasia; Infant, Premature; Oxygen; Superoxide Dismutase; Randomized Controlled Trials as Topic
PubMed: 37811631
DOI: 10.1002/14651858.CD013232.pub2 -
Antioxidants (Basel, Switzerland) Apr 2024Melatonin is an indoleamine with crucial antioxidant properties that are used to combat inflammatory and neoplastic processes, as well as control transplants. However,... (Review)
Review
UNLABELLED
Melatonin is an indoleamine with crucial antioxidant properties that are used to combat inflammatory and neoplastic processes, as well as control transplants. However, the clinical applications of melatonin have not yet been fully consolidated in the literature and require in-depth analysis.
OBJECTIVES
This study reviewed the literature on the antioxidant properties of melatonin in rat models.
METHODS
We followed the guidelines of the Preferred Reporting Items for Systematic Reviews and Meta-analyses and used the PubMed, LILACS, and Cochrane databases, Google Scholar, and article references, irrespective of publication time.
RESULTS
Ten articles involving 485 rats were selected, and the effects of melatonin on antioxidant markers were investigated. Melatonin increased superoxide dismutase in nine studies, glutathione peroxidase in seven studies, and catalase in five studies. In contrast, melatonin reduced glutathione in three studies and malonaldehyde in seven of eight studies.
CONCLUSION
Our findings suggest that melatonin effectively reduces oxidative stress.
PubMed: 38671887
DOI: 10.3390/antiox13040439 -
Phytotherapy Research : PTR Aug 2023Oxidative stress (OS) is a key factor involved in the initiation and development of chronic diseases. Despite its widespread acceptance as an antioxidant, the effects of... (Meta-Analysis)
Meta-Analysis Review
Oxidative stress (OS) is a key factor involved in the initiation and development of chronic diseases. Despite its widespread acceptance as an antioxidant, the effects of ginseng on OS in human clinical trials have not been comprehensively analyzed. Therefore, this study aimed to synthesize the results of previous randomized clinical trials (RCTs) examining the impact of ginseng consumption on OS indicators. PubMed, Web of Science, Scopus, and Cochrane databases were searched for articles on the effects of ginseng consumption on oxidative stress markers up to March 20, 2023. Standardized mean difference (SMD) and 95% confidence intervals (CIs) were used to assess effect sizes. Twelve RCTs with 15 effect sizes revealed that the effects of ginseng lowered serum malondialdehyde (MDA) levels (SMD = 0.45, 95% CI: -0.87, -0.08; p = 0.03) and significantly increased the serum total antioxidant capacity (TAC) (SMD = 0.23, 95% CI: 0.01, 0.45; p = 0.04), oxidative dismutase (SOD) (SMD = 0.39, 95% CI: 0.21, 0.57; p < 0.0001), glutathione (GSH) (SMD = 0.36; 95% CI: 0.11, 0.61; p = 0.005), and glutathione reductase (GR) (SMD = 0.56; 95% CI: 0.31, 0.81; p < 0.0001) levels compared to the effects of placebo. However, the effects on serum glutathione peroxidase (GPx) and catalase (CAT) were not significant. Moreover, subgroup analysis based on intervention duration showed that ginseng consumption increased GPx (SMD = 0.91, 95% CI: 0.05, 1.78; p = 0.039) and CAT (SMD = 0.74, 95% CI: 0.27, 1.21; p = 0.002) levels after more than 4 weeks of intervention. According to the results of this meta-analysis, ginseng supplementation dramatically reduced MDA levels and increased TAC, SOD, GSH, and GR levels. Our results open up a new line of defense against oxidative stress-induced diseases.
Topics: Humans; Antioxidants; Dietary Supplements; Panax; Oxidative Stress; Biomarkers; Glutathione Peroxidase; Superoxide Dismutase
PubMed: 37216939
DOI: 10.1002/ptr.7893 -
Nutrition Reviews Dec 2023Carnosine and histidine-containing dipeptides (HCDs) are suggested to have anti-inflammatory and antioxidative benefits, but their effects on circulating adipokines and...
CONTEXT
Carnosine and histidine-containing dipeptides (HCDs) are suggested to have anti-inflammatory and antioxidative benefits, but their effects on circulating adipokines and inflammatory and oxidative stress biomarkers remain unclear.
OBJECTIVES
The aim of the present systematic review and meta-analysis was to determine the impact of HCD supplementation on inflammatory and oxidative stress biomarkers.
DATA SOURCES
A systematic search was performed on Medline via Ovid, Scopus, Embase, ISI Web of Science, and the Cochrane Library databases from inception to 25 January 2023.
DATA EXTRACTION
Using relevant key words, trials investigating the effects of carnosine/HCD supplementation on markers of inflammation and oxidative stress, including C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), adiponectin, malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), total antioxidant capacity (TAC), and catalase (CAT) were identified. Meta-analyses were conducted using random-effects models to calculate the weighted mean differences (WMDs) and 95% confidence intervals (CIs).
DATA ANALYSIS
A total of 9 trials comprising 350 participants were included in the present meta-analysis. Carnosine/HCD supplementation led to a significant reduction in CRP (WMD: -0.97 mg/L; 95% CI: -1.59, -0.36), TNF-α (WMD: -3.60 pg/mL; 95% CI: -7.03, -0.18), and MDA (WMD: -0.34 μmol/L; 95% CI: -0.56, -0.12) and an elevation in CAT (WMD: 4.48 U/mL; 95% CI: 2.43, 6.53) compared with placebo. In contrast, carnosine/HCD supplementation had no effect on IL-6, adiponectin, GSH, SOD, and TAC levels.
CONCLUSION
Carnosine/HCD supplementation may reduce inflammatory and oxidative stress biomarkers, and potentially modulate the cardiometabolic risks associated with chronic low-grade inflammation and lipid peroxidation.
SYSTEMATIC REVIEW REGISTRATION
PROSPERO registration no. CRD42017075354.
PubMed: 38086332
DOI: 10.1093/nutrit/nuad150 -
Antioxidants (Basel, Switzerland) Oct 2023The aim of this meta-analysis is to explore all the available literature to obtain updated data about the potential use of antioxidants in the treatment of rheumatoid... (Review)
Review
OBJECTIVE
The aim of this meta-analysis is to explore all the available literature to obtain updated data about the potential use of antioxidants in the treatment of rheumatoid arthritis (RA) and its ability to reduce disease progression and cardiovascular risk.
METHODS
This systematic review and meta-analysis was performed strictly in accordance with the PRISMA guidelines. English and Chinese databases were searched with a retrieval time up to March 2023. These databases included the PubMed, Embase, Medline Complete, Web of Sciences and Cochrane Collaboration, Wanfang, China National Knowledge Infrastructure, and VIP databases. This literature search was formulated by the two researchers independently. The search strategy consists of reading, collecting the literature, and conducting the preliminary screening. After that, they provide the final selection of the literature according to the inclusion criteria and data extraction. Also, for all studies, the risk bias was assessed to evaluate the quality of the included references. The content of the risk assessment of bias included the following criteria: random allocation method, allocation plan hiding, blind method, completeness of result data, and selectivity of reporting of results, as well as other biases. The main outcomes were clinical efficiency of antioxidant therapy (C-reactive protein, DAS28 score, HAQ, Number of tender joints, etc.) and oxidative stress indicators (catalase, superoxide dismutase, or total antioxidant capacity).
RESULTS
We observed, in most of the studies, the small or moderate effects of antioxidant treatment. The mean effect size is 0.525, and that means that moderate effects were observed in 30 selected RCTs. Also, this effect is confirmed in the 1652 patients with RA with the mean confidence interval of 0.276 (lower limit) and 0.983 (upper limit). Cohen coefficient was calculated at 0.05.
CONCLUSION
The existing evidence is that antioxidants can reduce systemic and local oxidative stress and can reduce damage as the main agent involved in autoimmune diseases such as rheumatoid arthritis.
PubMed: 38001790
DOI: 10.3390/antiox12111938 -
Phytotherapy Research : PTR Sep 2023The present study aimed to assess the effect of propolis supplementation on oxidative status, a key contributor to the etiology of many chronic diseases. A systematic... (Meta-Analysis)
Meta-Analysis Review
The present study aimed to assess the effect of propolis supplementation on oxidative status, a key contributor to the etiology of many chronic diseases. A systematic search of multiple databases, including Web of Science, SCOPUS, Embase, PubMed, and Google Scholar, was conducted from inception to October 2022 to identify articles examining the effect of propolis on glutathione (GSH), glutathione peroxidase (GPX), total antioxidant capacity (TAC), superoxide dismutase (SOD), and malondialdehyde (MDA) levels. The quality of the included studies was evaluated using the Cochrane Collaboration tool. A total of nine studies were included in the final analysis, and a random-effects model was used to pool the estimated effects. Results showed that propolis supplementation significantly increased the levels of GSH (SMD = 3.16; 95% CI: 1.15, 5.18; I = 97.2%), GPX (SMD = 0.56; 95% CI: 0.07, 1.05; p = 0.025; I = 62.3%), and TAC (SMD = 3.26; 95% CI: 0.89, 5.62; I = 97.8%, p < 0.001). However, the effect of propolis on SOD was not significant (SMD = 0.05; 95% CI: -0.25, 0.34; I = 0.0%). Although the MDA concentration was not significantly decreased overall (SMD = -0.85, 95% CI: -1.70, 0.09; I = 93.3%), a significant decrease in MDA levels was observed at doses ≥1000 mg/day (SMD = -1.90; 95% CI: -2.97, -0.82; I = 86.4) and supplementation durations of less than 11 weeks (SMD = -1.56; 95% CI: -2.60, -0.51; I = 90.4). These results suggest that propolis is a safe supplement with a beneficial effect on GSH, GPX, and TAC levels and may be an effective adjunctive therapy for diseases where oxidative stress is a key factor in the etiology. However, further high-quality studies are necessary to make more precise and comprehensive recommendations given the limited number of studies, clinical diversity, and other limitations.
Topics: Antioxidants; Propolis; Dietary Supplements; Oxidative Stress; Superoxide Dismutase; Glutathione Peroxidase; Biomarkers
PubMed: 37317592
DOI: 10.1002/ptr.7899 -
Pharmaceuticals (Basel, Switzerland) Sep 2023The objective of this study is to assess the effectiveness of treatment for inflammatory bowel diseases in modulating oxidative stress biomarkers and cytokine levels. A... (Review)
Review
The objective of this study is to assess the effectiveness of treatment for inflammatory bowel diseases in modulating oxidative stress biomarkers and cytokine levels. A systematic review of clinical trials was conducted, searching electronic databases including PubMed, Science Direct, and Scopus. After excluding articles that did not meet the inclusion criteria, 19 studies were included in the systematic review and 8 in the meta-analysis (6 for antioxidant capacity, 6 for superoxide dismutase (SOD), and 5 for lipid peroxidation analyzed through malondialdehyde (MDA) levels). SOD was significantly modulated (RR = 0.3764, 95% CI [0.0262 to 0.7267], = 0.035) but not antioxidant capacity (RR = 0.3424, 95% CI [0.0334 to 0.7183], = 0.0742) or MDA (RR = -0.8534, 95% CI [-1.9333 to 0.2265], = 0.1214). Nonetheless, studies investigating oxidative stress biomarkers and cytokines in the context of alternative therapies for IBD treatment are still scarce. This review highlights the potential of antioxidant supplementation in IBD management and underscores the need for further investigations into its effects on oxidative stress biomarkers and cytokines to improve therapeutic approaches for IBD patients.
PubMed: 37895845
DOI: 10.3390/ph16101374 -
Journal of Ethnopharmacology Dec 2023Cerebral ischemia is a common disease that seriously threatens the health of human beings. Tanshinone IIA (TSA) is a fat-soluble compound isolated from the traditional... (Meta-Analysis)
Meta-Analysis Review
ETHNOPHARMACOLOGICAL RELEVANCE
Cerebral ischemia is a common disease that seriously threatens the health of human beings. Tanshinone IIA (TSA) is a fat-soluble compound isolated from the traditional Chinese medicine Danshen. Recent studies have shown that TSA plays a significant protective role in the animal models of cerebral ischemic injury.
AIM OF THE STUDY
The meta-analysis was to evaluate the protective effect of Danshen (Salvia miltiorrhiza Bunge) extract (TSA) in cerebral ischemic injury, aiming at providing scientific evidence for clinical application of TSA in the treatment of cerebral ischemia in patients.
MATERIALS AND METHODS
All relevant studies published in PubMed, Web of Science, Cochrane Library, China National Knowledge Infrastructure (CNKI), Wanfang Database, Chinese Scientific Journals Database (VIP) and Chinese Biomedicine Database (CBM) before Jan 2023 were systematically retrieved. The methodological quality was assessed by SYRCLE's risk of bias tool for the animal studies. Data was analyzed using Rev Man 5.3 software.
RESULTS
A total of 13 studies were included. Compared with the control group, TSA significantly reduced the expression of glial fibrillary acidic protein (GFAP) (mean difference [MD], -1.78; 95% CI, [-2.13, -1.44]; P < 0.00001) and high mobility group protein B1 (HMGB1) (MD, -0.69; 95% CI, [-0.87, -0.52]; P < 0.00001). TSA also inhibited the activation of brain nuclear factor κB (NF-κB) (MD, - 0.36; 95% CI, [-0.41, -0.32]; P < 0.00001), malondialdehyde (MDA) (MD, -0.90; 95% CI, [-1.66, -0.13]; P = 0.02), cysteine protease-3 (Caspase-3) (MD, -1.39; 95% CI, [-1.98, -0.81]; P < 0.00001), and reduced cerebral infarction volume(MD, -16.26; 95% CI, [-20.76, -11.77]; P < 0.00001), brain water content (MD, -4.89; 95% CI, [-7.06, -2.71]; P < 0.0001) and neurological deficit scores (MD, -1.19; 95% CI, [-1.48, -0.89]; P < 0.00001). Additionally, TSA increased the brain content of superoxide dismutase (SOD) (MD, 68.31; 95% CI, [10.41, 126.22]; P = 0.02).
CONCLUSIONS
The result of this study showed that TSA had a protective effect on cerebral ischemic injury in animal models, and the mechanism is associated with the reduction of inflammation and oxidative stress, and the inhibition of cell apoptosis. However, the quality of included studies may affect the accuracy of positive results. Therefore, more high-quality randomized controlled animal experiments are need for meta-analysis in the future.
Topics: Animals; Humans; Salvia miltiorrhiza; Brain Ischemia; Cerebral Infarction; Brain; Medicine, Chinese Traditional; Brain Injuries
PubMed: 37400004
DOI: 10.1016/j.jep.2023.116772