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Diagnostic Pathology Mar 2024Amyotrophic lateral sclerosis (ALS) is a progressive and fatal motor neuron disease. Due to the limited knowledge about potential biomarkers that help in early diagnosis... (Review)
Review
BACKGROUND
Amyotrophic lateral sclerosis (ALS) is a progressive and fatal motor neuron disease. Due to the limited knowledge about potential biomarkers that help in early diagnosis and monitoring disease progression, today's diagnoses are based on ruling out other diseases, neurography, and electromyography examination, which takes a time-consuming procedure.
METHODS
PubMed, ScienceDirect, and Web of Science were explored to extract articles published from January 2015 to June 2023. In the searching strategy following keywords were included; amyotrophic lateral sclerosis, biomarkers, cerebrospinal fluid, serum, and plama.
RESULTS
A total number of 6 studies describing fluid-based exosomal biomarkers were included in this study. Aggregated proteins including SOD1, TDP-43, pTDP-43, and FUS could be detected in the microvesicles (MVs). Moreover, TDP-43 and NFL extracted from plasma exosomes could be used as prognostic biomarkers. Also, downregulated miR-27a-3p detected through exoEasy Maxi and exoQuick Kit in the plasma could be measured as a diagnostic biomarker. Eventually, the upregulated level of CORO1A could be used to monitor disease progression.
CONCLUSION
Based on the results, each biomarker alone is insufficient to evaluate ALS. CNS-derived exosomes contain multiple ALS-related biomarkers (SOD1, TDP-43, pTDP-43, FUS, and miRNAs) that are detectable in cerebrospinal fluid and blood is a proper alternation. Exosome detecting kits listed as exoEasy, ExoQuick, Exo-spin, ME kit, ExoQuick Plus, and Exo-Flow, are helpful to reach this purpose.
Topics: Humans; Exosomes; Amyotrophic Lateral Sclerosis; Superoxide Dismutase-1; Biomarkers; DNA-Binding Proteins; Disease Progression
PubMed: 38429818
DOI: 10.1186/s13000-024-01473-6 -
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 -
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 2023Although several meta-analyses support the positive effect of coenzyme Q10 (CoQ10) on biomarkers of oxidative stress and inflammation, the results of some other studies...
Although several meta-analyses support the positive effect of coenzyme Q10 (CoQ10) on biomarkers of oxidative stress and inflammation, the results of some other studies reject such effects. Therefore, in this umbrella meta-analysis, we performed a comprehensive systematic search in such databases as Web of Science, PubMed, Scopus, Embase, and Google Scholar up to January 2023. Based on standardized mean difference analysis, CoQ10 supplementation significantly decreased serum C-reactive protein (CRP) (ES = -0.39; 95% CI: 0.77, -0.01, = 0.042) and malondialdehyde (MDA) (ES = -1.17; 95% CI: 1.55, -0.79, < 0.001), while it increased the total antioxidant capacity (TAC) (ES = 1.21; 95% CI: 0.61, 1.81, < 0.001) and serum superoxide dismutase (SOD) activity (ES = 1.08; 95% CI: 0.37, 1.79, = 0.003). However, CoQ10 supplementation had no significant reducing effect on tumor-necrosis factor-alpha (TNF- α) (ES = -0.70; 95% CI: 2.09, 0.68, = 0.320) and interleukin-6 (IL-6) levels (ES = -0.85; 95% CI: 1.71, 0.01, = 0.053). Based on weighted mean difference analysis, CoQ10 supplementation considerably decreased TNF-α (ES = -0.46, 95% CI: 0.65, -0.27; < 0.001), IL-6 (ES = -0.92, 95% CI: 1.40, -0.45; < 0.001), and CRP levels (effect sizes = -0.28, 95% CI: 0.47, -0.09; < 0.001). The results of our meta-analysis supported the alleviating effects of CoQ10 on markers of inflammation cautiously. However, CoQ10 had antioxidant effects regarding the improvement of all the studied antioxidant and oxidative stress biomarkers. https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=323861, identifier CRD42022323861.
PubMed: 37614320
DOI: 10.3389/fphar.2023.1191290 -
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 -
Ecotoxicology and Environmental Safety Nov 2023Oxidative stress (OS) constitutes a pivotal factor in the initiation and progression of lipopolysaccharide (LPS) challenges in broiler chickens. Increasing studies have... (Meta-Analysis)
Meta-Analysis Review
Oxidative stress (OS) constitutes a pivotal factor in the initiation and progression of lipopolysaccharide (LPS) challenges in broiler chickens. Increasing studies have demonstrated that Alleviation of oxidative stress seems to be a reasonable strategy to alleviate LPS-mediated afflictions in broilers. Nonetheless, the relationship between OS-related indicators and exposure to LPS remains a topic of debate. The aim of this investigation was to precisely and holistically evaluate the effect of LPS exposure on OS-associated markers. We conducted a systematic search of four electronic databases-PubMed, Web of Science, Scopus, and Cochrane for relevant studies, and a total of 31 studies were included. The overall results showed that the LPS treatment significantly increased the levels of oxygen radicals and their products, such as malondialdehydes (MDA), reactive oxygen species (ROS), and 8-hydroxy-2-deoxyguanosine (8-OHdG), while significantly reduced the levels of antioxidants, such as total antioxidative capacity (T-AOC), total superoxide dismutase (T-SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and glutathione (GSH), in the chickens. Intriguingly, though the observed trends in alterations were not strictly correlated with LPS concentrations, the enzyme activity levels were indeed influenced by the concentration of LPS. This observation highlights the complex relationship between LPS exposure and the body's antioxidant response. Despite some limitations, all the included studies were deemed credible. Subgroup evaluations revealed that the jejunum and duodenum has demonstrated stronger antioxidant capability compared to other tissues. Overall, our study presents compelling evidence that exposure to LPS induces significant OS in chickens. And we also found that the extent of OS was related to LPS doses, target tissues, and dietary ingredients.
Topics: Animals; Antioxidants; Chickens; Lipopolysaccharides; Oxidative Stress; Glutathione; Reactive Oxygen Species; 8-Hydroxy-2'-Deoxyguanosine; Biomarkers; Dietary Supplements
PubMed: 37866038
DOI: 10.1016/j.ecoenv.2023.115606 -
Lipids in Health and Disease Feb 2024Myocardial ischemia-reperfusion injury (MIRI) is widespread in the treatment of ischemic heart disease, and its treatment options are currently limited. Adiponectin... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Myocardial ischemia-reperfusion injury (MIRI) is widespread in the treatment of ischemic heart disease, and its treatment options are currently limited. Adiponectin (APN) is an adipocytokine with cardioprotective properties; however, the mechanisms of APN in MIRI are unclear. Therefore, based on preclinical (animal model) evidence, the cardioprotective effects of APN and the underlying mechanisms were explored.
METHODS
The literature was searched for the protective effect of APN on MIRI in six databases until 16 November 2023, and data were extracted according to selection criteria. The outcomes were the size of the myocardial necrosis area and hemodynamics. Markers of oxidation, apoptosis, and inflammation were secondary outcome indicators. The quality evaluation was performed using the animal study evaluation scale recommended by the Systematic Review Center for Laboratory animal Experimentation statement. Stata/MP 14.0 software was used for the summary analysis.
RESULTS
In total, 20 papers with 426 animals were included in this study. The pooled analysis revealed that APN significantly reduced myocardial infarct size [weighted mean difference (WMD) = 16.67 (95% confidence interval (CI) = 13.18 to 20.16, P < 0.001)] and improved hemodynamics compared to the MIRI group [Left ventricular end-diastolic pressure: WMD = 5.96 (95% CI = 4.23 to 7.70, P < 0.001); + dP/dtmax: WMD = 1393.59 (95% CI = 972.57 to 1814.60, P < 0.001); -dP/dtmax: WMD = 850.06 (95% CI = 541.22 to 1158.90, P < 0.001); Left ventricular ejection fraction: WMD = 9.96 (95% CI = 7.29 to 12.63, P < 0.001)]. Apoptosis indicators [caspase-3: standardized mean difference (SMD) = 3.86 (95% CI = 2.97 to 4.76, P < 0.001); TUNEL-positive cells: WMD = 13.10 (95% CI = 8.15 to 18.05, P < 0.001)], inflammatory factor levels [TNF-α: SMD = 4.23 (95% CI = 2.48 to 5.98, P < 0.001)], oxidative stress indicators [Superoxide production: SMD = 4.53 (95% CI = 2.39 to 6.67, P < 0.001)], and lactate dehydrogenase levels [SMD = 2.82 (95% CI = 1.60 to 4.04, P < 0.001)] were significantly reduced. However, the superoxide dismutase content was significantly increased [SMD = 1.91 (95% CI = 1.17 to 2.65, P < 0.001)].
CONCLUSION
APN protects against MIRI via anti-inflammatory, antiapoptotic, and antioxidant effects, and this effect is achieved by activating different signaling pathways.
Topics: Rats; Animals; Myocardial Reperfusion Injury; Rats, Sprague-Dawley; Adiponectin; Myocardial Infarction; Signal Transduction; Apoptosis
PubMed: 38368320
DOI: 10.1186/s12944-024-02028-w -
Reproductive Biology and Endocrinology... Apr 2024Metformin is an insulin sensitizer that is widely used for the treatment of insulin resistance in polycystic ovary syndrome patients. However, metformin can cause... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Metformin is an insulin sensitizer that is widely used for the treatment of insulin resistance in polycystic ovary syndrome patients. However, metformin can cause gastrointestinal side effects.
PURPOSE
This study showed that the effects of quercetin are comparable to those of metformin. Therefore, this study aimed to systematically evaluate the efficacy of quercetin in treating PCOS.
METHODS
The present systematic search of the Chinese National Knowledge Infrastructure (CNKI), Wanfang Data Information Site, Chinese Scientific Journals Database (VIP), SinoMed, Web of Science, and PubMed databases was performed from inception until February 2024. The methodological quality was then assessed by SYRCLE's risk of bias tool, and the data were analyzed by RevMan 5.3 software.
RESULTS
Ten studies were included in the meta-analysis. Compared with those in the model group, quercetin in the PCOS group had significant effects on reducing fasting insulin serum (FIS) levels (P = 0.0004), fasting blood glucose (FBG) levels (P = 0.01), HOMA-IR levels (P < 0.00001), cholesterol levels (P < 0.0001), triglyceride levels (P = 0.001), testosterone (T) levels (P < 0.00001), luteinizing hormone (LH) levels (P = 0.0003), the luteinizing hormone/follicle stimulating hormone (LH/FSH) ratio (P = 0.01), vascular endothelial growth factor (VEGF) levels (P < 0.00001), malondialdehyde (MDA) levels (P = 0.03), superoxide dismutase (SOD) levels (P = 0.01) and GLUT4 mRNA expression (P < 0.00001).
CONCLUSION
This meta-analysis suggested that quercetin has positive effects on PCOS treatment. Quercetin can systematically reduce insulin, blood glucose, cholesterol, and triglyceride levels in metabolic pathways. In the endocrine pathway, quercetin can regulate the function of the pituitary-ovarian axis, reduce testosterone and luteinizing hormone (LH) levels, and lower the ratio of LH to follicle-stimulating hormone (FSH). Quercetin can regulate the expression of the GLUT4 gene and has antioxidative effects at the molecular level.
Topics: Female; Animals; Humans; Polycystic Ovary Syndrome; Quercetin; Blood Glucose; Vascular Endothelial Growth Factor A; Luteinizing Hormone; Insulin; Follicle Stimulating Hormone; Metformin; Insulin Resistance; Testosterone; Cholesterol; Triglycerides
PubMed: 38637876
DOI: 10.1186/s12958-024-01220-y -
PloS One 2024This study aimed to evaluate the intervention effect of curcumin on hepatic fibrosis in rodent models through systematic review and meta-analysis, in order to provide... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVE
This study aimed to evaluate the intervention effect of curcumin on hepatic fibrosis in rodent models through systematic review and meta-analysis, in order to provide meaningful guidance for clinical practice.
METHODS
A systematic retrieval of relevant studies on curcumin intervention in rats or mice hepatic fibrosis models was conducted, and the data were extracted. The outcome indicators included liver cell structure and function related indicators, such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), albumin (ALB), ratio of albumin to globulin (A/G), total bilirubin (TBIL), bax protein, bcl-2 protein and index of liver, as well as the relevant indicators for evaluating the degree of hepatic fibrosis, such as hyaluronic acid (HA), laminin (LN), type I collagen (Collagen I), type III collagen (Collagen III), type III procollagen (PCIII), type III procollagen amino terminal peptide (PIIINP), type IV collagen (IV-C), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), α-Smooth muscle actin (α-SMA), hydroxyproline (HYP), platelet derived factor-BB (PDGF-BB), connective tissue growth factor (CTGF) and transforming growth factor-β1 (TGF-β1), and oxidative stress-related indicators, such as superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px). These results were then analyzed by meta-analysis. Studies were evaluated for methodological quality using the syrcle's bias risk tool.
RESULTS
A total of 59 studies were included in the meta-analysis, and the results showed that curcumin can reduce the levels of ALT, AST, ALP, TBIL, bax protein, and index of liver in hepatic fibrosis models. It can also reduce HA, LN, Collagen I, Collagen III, PCIII, PIIINP, IV-C, TNF-α, α-SMA, HYP, PDGF-BB, CTGF, TGF-β1 and MDA, and increase the levels of ALB, A/G, SOD, and GSH-Px in the hepatic fibrosis models. However, the effects of curcumin on bcl-2 protein, IL-6 in hepatic fibrosis models and index of liver in mice were not statistically significant.
CONCLUSION
The analysis results indicate that curcumin can reduce liver cell apoptosis by maintaining the stability of liver cell membrane, inhibit the activation and proliferation of hepatic stellate cells by reducing inflammatory response, and alleviate tissue peroxidation damage by clearing oxygen free radicals.
Topics: Animals; Liver Cirrhosis; Curcumin; Mice; Rats; Disease Models, Animal; Oxidative Stress; Liver
PubMed: 38781262
DOI: 10.1371/journal.pone.0304176 -
Nutrients Jul 2023Stevia ( Bertoni) is an aromatic plant known for its high sweetening power ascribed to its glycosides. Stevia also contains several bioactive compounds showing... (Meta-Analysis)
Meta-Analysis Review
Stevia ( Bertoni) is an aromatic plant known for its high sweetening power ascribed to its glycosides. Stevia also contains several bioactive compounds showing antioxidant, antiproliferative, antimicrobial, and anti-inflammatory activities. Since inflammation and oxidative stress play critical roles in the pathogenesis of many diseases, stevia emerges as a promising natural product that could support human health. In this study we set out to investigate the way stevia affects oxidative stress markers (e.g., SOD, CAT, GPx, GSH, MDA) in diseased rats administered stevia leaf extracts or glycosides. To this end, we performed an inclusive literature search, following PRISMA guidelines, and recruited multivariate meta-analysis and meta-regression to synthesize all available data on experimental animal models encountering (a) healthy, (b) diseased, and (c) stevia-treated diseased rats. From the 184 articles initially retrieved, 24 satisfied the eligibility criteria, containing 104 studies. Our results demonstrate that regardless of the assay employed, stevia leaf extracts restored all oxidative stress markers to a higher extent compared to pure glycosides. Meta-regression analysis revealed that results from SOD, CAT, GSH, and TAC assays are not statistically significantly different ( = 0.184) and can be combined in meta-analysis. Organic extracts from stevia leaves showed more robust antioxidant properties compared to aqueous or hydroalcoholic ones. The restoration of oxidative markers ranged from 65% to 85% and was exhibited in all tested tissues. Rats with diabetes mellitus were found to have the highest restorative response to stevia leaf extract administration. Our results suggest that stevia leaf extract can act protectively against various diseases through its antioxidant properties. However, which of each of the multitude of stevia compounds contribute to this effect, and to what extent, awaits further investigation.
Topics: Humans; Rats; Animals; Antioxidants; Stevia; Plant Extracts; Glycosides; Superoxide Dismutase; Plant Leaves
PubMed: 37571265
DOI: 10.3390/nu15153325