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Frontiers in Medicine 2023This study aimed to perform an updated systematic review and meta-analysis to evaluate the effectiveness of saffron supplementation on oxidative stress markers...
Effect of saffron supplementation on oxidative stress markers (MDA, TAC, TOS, GPx, SOD, and pro-oxidant/antioxidant balance): An updated systematic review and meta-analysis of randomized placebo-controlled trials.
INTRODUCTION
This study aimed to perform an updated systematic review and meta-analysis to evaluate the effectiveness of saffron supplementation on oxidative stress markers [malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS), glutathione peroxidase (GPx), superoxide dismutase (SOD), and prooxidant/antioxidant balance (PAB)] in randomized controlled trials (RCTs).
METHODS
We searched PubMed/Medline, Web of Science, Scopus, Cochrane CENTRAL, and Google Scholar until December 2022. Trial studies investigating the effects of oral saffron supplements on MDA, TAC, TOS, GPx, SOD, and PAB concentrations were included in the study. To analyze the results, mean differences (SMD) and 95% confidence intervals (CI) were pooled using a random effects model. Heterogeneity was assessed using the Cochrane and values. Sixteen cases were included in the meta-analysis (468 and 466 subjects in the saffron and control groups, respectively).
RESULTS
It was found that saffron consumption caused a significant decrease in MDA (SMD: -0.322; 95% CI: -0.53, -0.16; = 32.58%) and TOS (SMD: -0.654; 95% CI: -1.08, -0.23; = 68%) levels as well as a significant increase in TAC (SMD: 0.302; 95% CI: 0.13, 0.47; = 10.12%) and GPx (SMD: 0.447; 95% CI: 0.10, 0.80; = 35%). Subgroup analysis demonstrated a significant reduction in MDA levels in studies with a saffron dosage of >30 mg/day, age of <50 years, and study duration of <12 weeks. Among the limitations of the study, we can point out that the studies were from Iran, the different nature of the diseases included, and were not considered of some potential confounders such as smoking, physical activity, and diet in the studies.
DISCUSSION
In summary, the results showed that saffron has beneficial effects on oxidative stress markers.
PubMed: 36817799
DOI: 10.3389/fmed.2023.1071514 -
Antioxidants (Basel, Switzerland) Aug 2023Sleep deprivation is highly prevalent in the modern world, possibly reaching epidemic proportions. While multiple theories regarding the roles of sleep exist... (Review)
Review
Sleep deprivation is highly prevalent in the modern world, possibly reaching epidemic proportions. While multiple theories regarding the roles of sleep exist (inactivity, energy conservation, restoration, brain plasticity and antioxidant), multiple unknowns still remain regarding the proposed antioxidant roles of sleep. The existing experimental evidence is often contradicting, with studies pointing both toward and against the presence of oxidative stress after sleep deprivation. The main goals of this review were to analyze the existing experimental data regarding the relationship between sleep deprivation and oxidative stress, to attempt to further clarify multiple aspects surrounding this relationship and to identify current knowledge gaps. Systematic searches were conducted in three major online databases for experimental studies performed on rat models with oxidative stress measurements, published between 2015 and 2022. A total of 54 studies were included in the review. Most results seem to point to changes in oxidative stress parameters after sleep deprivation, further suggesting an antioxidant role of sleep. Alterations in these parameters were observed in both paradoxical and total sleep deprivation protocols and in multiple rat strains. Furthermore, the effects of sleep deprivation seem to extend beyond the central nervous system, affecting multiple other body sites in the periphery. Sleep recovery seems to be characterized by an increased variability, with the presence of both normalizations in some parameters and long-lasting changes after sleep deprivation. Surprisingly, most studies revealed the presence of a stress response following sleep deprivation. However, the origin and the impact of the stress response during sleep deprivation remain somewhat unclear. While a definitive exclusion of the influence of the sleep deprivation protocol on the stress response is not possible, the available data seem to suggest that the observed stress response may be determined by sleep deprivation itself as opposed to the experimental conditions. Due to this fact, the observed oxidative changes could be attributed directly to sleep deprivation.
PubMed: 37627596
DOI: 10.3390/antiox12081600 -
Frontiers in Pharmacology 2023Potentilla discolor Bunge (PDB) is an ancient herb of traditional Chinese medicine. Studies have suggested that extracts of PDB may ameliorate diabetes mellitus (DM)....
Potentilla discolor Bunge (PDB) is an ancient herb of traditional Chinese medicine. Studies have suggested that extracts of PDB may ameliorate diabetes mellitus (DM). This study aimed to systematically assess the efficacy of PDB extracts on glycolipid metabolism and oxidative stress in animal models of diabetes and to provide evidence-based references for the use of PDB extracts. This study followed the PRISMA 2020 guidelines. Studies were searched from eight databases until January 2023. Statistical analysis was performed using StataSE 15.0 and RevMan 5.3. The standard mean difference (SMD) and 95% confidence intervals (CI) were computed using the random-effects model. SYRCLE's risk of bias tool was used to assess the risk of bias. In total, 32 studies with 574 animals were included. The findings demonstrated that PDB extracts considerably lowered fasting blood glucose (SMD: -3.56, 95%CI: -4.40 to -2.72, < 0.00001); insulin resistance (SMD: -3.19, 95% CI: -5.46 to -0.92, = 0.006), total cholesterol (SMD: -2.18, 95%CI: -2.89 to -1.46, < 0.00001), triglyceride (SMD: -1.48, 95% CI: -2.01 to -0.96, < 0.00001), low-density lipoprotein cholesterol (SMD: -1.80, 95% CI: -2.58 to -1.02], < 0.00001), malondialdehyde (SMD: -3.46, 95% CI: -4.64 to -2.29, < 0.00001) and free fatty acid levels (SMD: -3.25, 95%CI: -5.33 to -1.16, = 0.002), meanwhile, increased insulin sensitivity index (SMD: 2.51 95% CI: 1.10 to 3.92, = 0.0005), body weight (SMD:1.20, 95% CI: 0.38 to 2.01, = 0.004), and the levels of high-density lipoprotein cholesterol (SMD: 1.04, 95% CI: 0.40 to 1.69, = 0.001), superoxide dismutase (SMD:2.63, 95% CI: 1.53 to 3.73, < 0.00001), glutathione peroxidase (SMD:1.13, 95%CI: 0.42 to1.83, = 0.002), and catalase (SMD:0.75, 95% CI: 0.11 to 1.40], = 0.02). These findings suggest that PDB extracts can ameliorate DM by improving glycolipid metabolism and oxidative stress. PDB may be a promising medication for DM; however, due to significant heterogeneity between studies, these findings should be interpreted with caution. In addition, future well-designed trials should determine which components of the PDB play a major role in ameliorating DM and whether these benefits persist in humans. https://www.crd.york.ac.uk/prospero, CRD42023379391.
PubMed: 37849729
DOI: 10.3389/fphar.2023.1218757 -
Journal of Neuroscience Research Dec 2022Neonatal encephalopathy (NE) that purportedly arises from hypoxia-ischemia is labeled hypoxic-ischemic encephalopathy (HIE). Perinatal asphyxia is a clinical syndrome... (Review)
Review
A systematic review of noninflammatory cerebrospinal fluid biomarkers for clinical outcome in neonates with perinatal hypoxic brain injury that could be biologically significant.
Neonatal encephalopathy (NE) that purportedly arises from hypoxia-ischemia is labeled hypoxic-ischemic encephalopathy (HIE). Perinatal asphyxia is a clinical syndrome involving acidosis, a low Apgar score and the need for resuscitation in the delivery room; asphyxia alerts one to the possibility of NE. In the present systematic review, we focused on the noninflammatory biomarkers in cerebrospinal fluid (CSF) that are involved in the development of possible brain injury in asphyxia or HIE. A literature search in PubMed and EMBASE for case-control studies was conducted and 17 studies were found suitable by a priori criteria. Statistical analysis used the Mantel-Haenszel model for dichotomous data. The pooled mean difference and 95% confidence intervals (CIs) were determined. We identified the best biomarkers, based on the estimation approach in evaluating the biological significance, out of hundreds in three categories: cell adhesion and proliferation, oxidants and antioxidants, and cell damage. The following subtotal-population comparisons were made: perinatal asphyxia versus no asphyxia, asphyxia with HIE versus asphyxia without HIE, asphyxia with HIE versus no asphyxia, and term versus preterm HIE newborn with asphyxia. Biological significance of the biomarkers was determined by using a modification of the estimation approach, by ranking the biomarkers according to the difference in the bounds of the CIs. The most promising CSF biomarkers for prognostication especially for the severest HIE include creatine kinase, xanthine oxidase, vascular endothelial growth factor, neuron-specific enolase, superoxide dismutase, and malondialdehyde. Future studies are recommended using such a combined test to prognosticate the most severely affected patients.
Topics: Female; Humans; Infant, Newborn; Pregnancy; Asphyxia Neonatorum; Biomarkers; Creatine Kinase; Hypoxia; Hypoxia-Ischemia, Brain; Malondialdehyde; Oxidants; Phosphopyruvate Hydratase; Superoxide Dismutase; Vascular Endothelial Growth Factor A; Xanthine Oxidase
PubMed: 33543500
DOI: 10.1002/jnr.24801 -
PloS One 2023The purpose of this review was to analyze the acute effects of low-load resistance exercise with blood flow restriction (LLE-BFR) on oxidative stress markers in healthy... (Meta-Analysis)
Meta-Analysis
BACKGROUND
The purpose of this review was to analyze the acute effects of low-load resistance exercise with blood flow restriction (LLE-BFR) on oxidative stress markers in healthy individuals in comparison with LLE or high-load resistance exercise (HLRE) without BFR.
MATERIALS AND METHODS
A systematic review was performed in accordance with the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. These searches were performed in CENTRAL, SPORTDiscus, EMBASE, PubMed, CINAHL and Virtual Health Library- VHL, which includes Lilacs, Medline and SciELO. The risk of bias and quality of evidence were assessed through the PEDro scale and GRADE system, respectively.
RESULTS
Thirteen randomized clinical trials were included in this review (total n = 158 subjects). Results showed lower post-exercise damage to lipids (SMD = -0.95 CI 95%: -1.49 to -0. 40, I2 = 0%, p = 0.0007), proteins (SMD = -1.39 CI 95%: -2.11 to -0.68, I2 = 51%, p = 0.0001) and redox imbalance (SMD = -0.96 CI 95%: -1.65 to -0.28, I2 = 0%, p = 0.006) in favor of LLRE-BFR compared to HLRE. HLRE presents higher post-exercise superoxide dismutase activity but in the other biomarkers and time points, no significant differences between conditions were observed. For LLRE-BFR and LLRE, we found no difference between the comparisons performed at any time point.
CONCLUSIONS
Based on the available evidence from randomized trials, providing very low or low certainty of evidence, this review demonstrates that LLRE-BFR promotes less oxidative stress when compared to HLRE but no difference in levels of oxidative damage biomarkers and endogenous antioxidants between LLRE.
TRIAL REGISTRATION
Register number: PROSPERO number: CRD42020183204.
Topics: Humans; Resistance Training; Exercise; Hemodynamics; Oxidative Stress; Biomarkers
PubMed: 37083560
DOI: 10.1371/journal.pone.0283237 -
Frontiers in Cardiovascular Medicine 2023Oxidative stress induced by the excessive production of reactive oxygen species is one of the primary mechanisms implicated in anthracycline (ANT)-induced... (Review)
Review
BACKGROUND
Oxidative stress induced by the excessive production of reactive oxygen species is one of the primary mechanisms implicated in anthracycline (ANT)-induced cardiotoxicity. There is a strong clinical need for a molecule capable of effectively preventing and reducing the oxidative damage caused by ANT. In vitro and studies conducted in mice have shown that melatonin stimulates the expression of antioxidative agents and reduces lipid peroxidation induced by ANT.
METHODS
We investigated this issue through a meta-analysis of murine model studies. The outcome of the meta-analysis was to compare oxidative damage, estimated by products of lipid peroxidation (MDA = Malondialdehyde) and markers of oxidative stress (SOD = Superoxide Dismutase, GSH = Glutathione), along with a marker of cardiac damage (CK-MB = creatine kinase-myocardial band), assessed by measurements in heart and/or blood samples in mice undergoing ANT chemotherapy and assuming melatonin vs. controls. The PubMed, OVID-MEDLINE and Cochrane library databases were analysed to search English-language review papers published from the inception up to August 1st, 2023. Studies were identified by using Me-SH terms and crossing the following terms: "melatonin", "oxidative stress", "lipid peroxidation", "anthracycline", "cardiotoxicity".
RESULTS
The metanalysis included 153 mice administered melatonin before, during or immediately after ANT and 153 controls from 13 studies. Compared with controls, the levels of all oxidative stress markers were significantly better in the pooled melatonin group, with standardized mean differences (SMD) for MDA, GSH and SOD being -8.03 ± 1.2 (CI: -10.43/-5.64, < 0.001), 7.95 ± 1.8 (CI: 4.41/11.5, < 0.001) and 3.94 ± 1.6 (CI: 0.77/7.12, = 0.015) respectively. Similarly, compared with controls, CK-MB levels reflecting myocardial damage were significantly lower in the pooled melatonin group, with an SMD of -4.90 ± 0.5 (CI: -5.82/-3.98, < 0.001).
CONCLUSION
Melatonin mitigates the oxidative damage induced by ANT in mouse model. High-quality human clinical studies are needed to further evaluate the use of melatonin as a preventative/treatment strategy for ANT-induced cardiotoxicity.
PubMed: 38075951
DOI: 10.3389/fcvm.2023.1289384 -
Frontiers in Pharmacology 2022This study aimed to evaluate the intervention effect of curcumin in myocardial infarction rodent models. A systematic retrieval of relevant studies on curcumin...
This study aimed to evaluate the intervention effect of curcumin in myocardial infarction rodent models. A systematic retrieval of relevant studies on curcumin intervention in rats or mice myocardial infarction models was conducted, and the data were extracted. The outcome indicators included biochemical blood indicators, such as creatine kinase (CK), creatine kinase isoenzyme (CK-MB), malondialdehyde (MDA), lactate dehydrogenase (LDH) and superoxide dismutase (SOD), as well as cardiac tissue structure indicators, such as left ventricular weight to body weight ratio (LVW/BW), apoptosis index, left ventricular end-diastolic dimension (LVEDD), left ventricular end-systolic diameter (LVESD), and myocardial infarction area, and hemodynamic indexes, such as systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular end-diastolic pressure (LVEDP), left ventricular ejection fraction (LVEF), left ventricular fractional shortening (LVFS), maximum rate of left ventricular pressure rise (+dp/dtmax), and maximum rate of left ventricular pressure decline (-dp/dtmax). These results were then analyzed by meta-analysis. Studies were evaluated for methodological quality using the syrcle's bias risk tool. A total of 24 studies were included in the meta-analysis. The quality assessment of included studies revealed that the evidence was low quality and none of studies was judged as having a low risk of bias across all domains. The results revealed that curcumin could reduce CK-MB, CK, LDH, and MDA levels. They also revealed that it could lower SBP, DBP, LVEDP, LVW/BW, apoptosis index, LVEDD, LVESD, and myocardial infarction area and increase LVEF, LVFS, +dp/dtmax, and-dp/dtmax. However, it had no significant impact on the heart rate and the levels of SOD in the models. Curcumin alleviates myocardial injury and oxidative stress in myocardial infarction rodent models in terms of blood biochemistry indicators, improves the diastolic and systolic capacity of the ventricle in terms of hemodynamic indexes, and reduces the necrosis and apoptosis of cardiomyocytes in terms of tissue structure. The methodological quality of the studies was low and additional research is warranted.
PubMed: 36330084
DOI: 10.3389/fphar.2022.999386 -
Frontiers in Nutrition 2022Nanomaterials, widely applied in various fields, are reported to have toxic effects on human beings; thus, preventive or therapeutic measures are urgently needed. Given...
BACKGROUND
Nanomaterials, widely applied in various fields, are reported to have toxic effects on human beings; thus, preventive or therapeutic measures are urgently needed. Given the anti-inflammatory and antioxidant activities, supplementation with flavonoids that are abundant in the human diet has been suggested as a potential strategy to protect against nanomaterial-induced toxicities. However, the beneficial effects of flavonoids remain inconclusive. In the present study, we performed a meta-analysis to comprehensively explore the roles and mechanisms of flavonoids for animals intoxicated with nanomaterials.
METHODS
A systematic literature search in PubMed, EMBASE, and Cochrane Library databases was performed up to April 2022. STATA 15.0 software was used for meta-analyses.
RESULTS
A total of 26 studies were identified. The results showed that flavonoid supplementation could significantly increase the levels of antioxidative enzymes (superoxide dismutase, catalase, glutathione, glutathione peroxidase, and glutathione-S-transferase), reduce the production of oxidative agents (malonaldehyde) and pro-inflammatory mediators (tumor necrosis factor-α, interleukin-6, IL-1β, C-reactive protein, immunoglobulin G, nitric oxide, vascular endothelial growth factor, and myeloperoxidase), and alleviate cell apoptosis (manifested by decreases in the mRNA expression levels of pro-apoptotic factors, such as caspase-3, Fas cell surface death receptor, and Bax, and increases in the mRNA expression levels of Bcl2), DNA damage (reductions in tail length and tail DNA%), and nanomaterial-induced injuries of the liver (reduced alanine aminotransferase and aspartate aminotransferase activities), kidney (reduced urea, blood urea nitrogen, creatinine, and uric acid concentration), testis (increased testosterone, sperm motility, 17β-hydroxysteroid dehydrogenase type, and reduced sperm abnormalities), and brain (enhanced acetylcholinesterase activities). Most of the results were not changed by subgroup analyses.
CONCLUSION
Our findings suggest that appropriate supplementation of flavonoids may be effective to prevent the occupational detriments resulting from nanomaterial exposure.
PubMed: 35774549
DOI: 10.3389/fnut.2022.929343 -
Oxidative Medicine and Cellular... 2021Maternal exposure to the high-fat diet (HFD) during gestation or lactation can be harmful to both a mother and offspring. The aim of this systematic review was to... (Meta-Analysis)
Meta-Analysis
Maternal exposure to the high-fat diet (HFD) during gestation or lactation can be harmful to both a mother and offspring. The aim of this systematic review was to identify and evaluate the studies with animal models (rodents) that were exposed to the high-fat diet during pregnancy and/or lactation period to investigate oxidative stress and lipid and liver enzyme profile of mothers and their offspring. The electronic search was performed in the PUBMED (Public/Publisher MEDLINE), EMBASE (Ovid), and Web of Science databases. Data from 77 studies were included for qualitative analysis, and of these, 13 studies were included for meta-analysis by using a random effects model. The pooled analysis revealed higher malondialdehyde levels in offspring of high-fat diet groups. Furthermore, the pooled analysis showed increased reactive oxygen species and lower superoxide dismutase and catalase in offspring of mothers exposed to high-fat diet during pregnancy and/or lactation. Despite significant heterogeneity, the systematic review shows oxidative stress in offspring induced by maternal HFD.
Topics: Animals; Diet, High-Fat; Female; Mice; Oxidative Stress; Pregnancy; Rats; Rodentia
PubMed: 34868458
DOI: 10.1155/2021/9073859 -
Frontiers in Pharmacology 2023Liver injury is a severe liver lesion caused by various etiologies and is one of the main areas of medical research. C.A. Meyer has traditionally been used as medicine... (Review)
Review
Liver injury is a severe liver lesion caused by various etiologies and is one of the main areas of medical research. C.A. Meyer has traditionally been used as medicine to treat diseases and regulate body functions. Ginsenosides are the main active components of ginseng, and their effects on liver injury have been extensively reported. Preclinical studies meeting the inclusion criteria were retrieved from PubMed, Web of Science, Embase, China National Knowledge Infrastructure (CNKI), and Wan Fang Data Knowledge Service Platforms. The Stata 17.0 was used to perform the meta-analysis, meta-regression, and subgroup analysis. This meta-analysis included ginsenosides Rb1, Rg1, Rg3, and compound K (CK), in 43 articles. The overall results showed that multiple ginsenosides significantly reduced alanine aminotransferase (ALT) and aspartate aminotransferase (AST), affected oxidative stress-related indicators, such as superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GSH-Px), and catalase (CAT), and reduced levels of inflammatory factor, such as factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6). Additionally, there was a large amount of heterogeneity in the meta-analysis results. Our predefined subgroup analysis shows that the animal species, the type of liver injury model, the duration of treatment, and the administration route may be the sources of some of the heterogeneity. In a word, ginsenosides have good efficacy against liver injury, and their potential mechanisms of action target antioxidant, anti-inflammatory and apoptotic-related pathways. However, the overall methodological quality of our current included studies was low, and more high-quality studies are needed to confirm their effects and mechanisms further.
PubMed: 37251340
DOI: 10.3389/fphar.2023.1184774