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Biochimica Et Biophysica Acta.... Nov 2023This study aims to explore the potential biomarkers in the development of diabetes mellitus (DM) into diabetic retinopathy (DR).
Integration of systematic review, lipidomics with experiment verification reveals abnormal sphingolipids facilitate diabetic retinopathy by inducing oxidative stress on RMECs.
OBJECTIVE
This study aims to explore the potential biomarkers in the development of diabetes mellitus (DM) into diabetic retinopathy (DR).
METHODS
Systematic review of diabetic metabolomics was used to screen the differential metabolites and related pathways during the development of DM. Non-targeted lipidomics of rat plasma was performed to explore the differential metabolites in the development of DM into DR in vivo. To verify the effects of differential metabolites in inducing retinal microvascular endothelial cells (RMECs) injury by increasing oxidative stress, high glucose medium containing differential metabolites was used to induce rat RMECs injury and cell viability, malondialdehyde (MDA) contents, superoxide dismutase (SOD) activities, reactive oxygen species (ROS) levels and mitochondrial membrane potential (MMP) were evaluated in vitro. Network pharmacology was performed to explore the potential mechanism of differential metabolites in inducing DR.
RESULTS
Through the systematic review, 148 differential metabolites were obtained and the sphingolipid metabolic pathway attracted our attention. Plasma non-targeted lipidomics found that sphingolipids were accompanied by the development of DM into DR. In vitro experiments showed sphinganine and sphingosine-1-phosphate aggravated rat RMECs injury induced by high glucose, further increased MDA and ROS levels, and further decreased SOD activities and MMP. Network pharmacology revealed sphinganine and sphingosine-1-phosphate may induce DR by regulating the AGE-RAGE and HIF-1 signaling pathways.
CONCLUSIONS
Integrated systematic review, lipidomics and experiment verification reveal that abnormal sphingolipid metabolism facilitates DR by inducing oxidative stress on RMECs. Our study could provide the experimental basis for finding potential biomarkers for the diagnosis and treatment of DR.
Topics: Rats; Animals; Diabetic Retinopathy; Reactive Oxygen Species; Sphingolipids; Lipidomics; Endothelial Cells; Oxidative Stress; Glucose; Superoxide Dismutase; Biomarkers; Diabetes Mellitus
PubMed: 37659619
DOI: 10.1016/j.bbalip.2023.159382 -
Phytotherapy Research : PTR Mar 2022Fatty liver disease (FLD) is the most common chronic liver disease worldwide. The pathogenesis of this disease is closely related to obesity and insulin resistance.... (Meta-Analysis)
Meta-Analysis Review
Fatty liver disease (FLD) is the most common chronic liver disease worldwide. The pathogenesis of this disease is closely related to obesity and insulin resistance. Ginger has hypolipidemic and antioxidant effects and acts as an insulin sensitizer. This study aims to evaluate the effect of ginger supplementation on the fatty liver. A comprehensive search of Medline/PubMed, Embase, Scopus, Web of Science/ISI, and Cochrane databases was conducted without time or language restrictions. Eighteen eligible studies were identified, including 17 in-vivo experiments in quantitative analysis and 3 clinical trials in qualitative analysis. The present study provides comprehensive evidence of the efficacy of ginger to improve the liver levels of cholesterol (-5.60 mg/g), triglycerides (TG, -4.28 mg/g), malondialdehyde (-3.16 nmol/mg), catalase (CAT) (3.35 nmol/mg), superoxide dismutase (SOD, 3.01 U/mg), serum levels of alanine aminotransferase (ALT, -2.85 U/L), aspartate aminotransferase (AST, -0.98 U/L), TG (-4.98 mg/dL), low-density lipoprotein (LDL, -3.94 mg/dL), total cholesterol (TC, -3.45 mg/dL), high-density lipoprotein (HDL, 1.27 mg/dL), and fasting blood sugar (FBS, -2.54 mg/dL). Ginger administration may reduce many clinical aspects of FLD by several mechanisms, including insulin-sensitive effects, stimulating the expression of antioxidant enzymes, reducing the generation of reactive oxygen species (ROS), having antidyslipidemic activities, and reducing hepatic fat content. However, future clinical trials are essential to investigate the clinical application of ginger in this area.
Topics: Alanine Transaminase; Aspartate Aminotransferases; Fatty Liver; Zingiber officinale; Humans; Liver; Non-alcoholic Fatty Liver Disease
PubMed: 35106852
DOI: 10.1002/ptr.7390 -
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 -
Nutrition Research (New York, N.Y.) Mar 2022Previous in vitro and animal studies showed that astaxanthin improved oxidative stress and inflammation biomarkers. We hypothesized the same effects of astaxanthin in... (Meta-Analysis)
Meta-Analysis Review
Previous in vitro and animal studies showed that astaxanthin improved oxidative stress and inflammation biomarkers. We hypothesized the same effects of astaxanthin in humans and conducted a systematic review and meta-analysis of previous randomized controlled trials to test this hypothesis. The literature search was performed on PubMed, Cochrane Library, and Scopus databases from January 1970 to April 2021. Main eligibility criteria include: intervention using astaxanthin for at least 1 week; inclusion of placebo control; and measuring at least 1 of the common oxidative stress and inflammation biomarkers before and after intervention. Twelve randomized controlled trials including 380 participants were included. Compared with placebo, astaxanthin significantly reduced blood malondialdehyde concentration (standardized mean difference [SMD]: -0.95; 95% CI, -1.67 to -0.23; P = .01). The lowering effect of astaxanthin supplementation on malondialdehyde was particularly significant in type 2 diabetes mellitus (T2DM) patients (SMD: -0.64; 95% CI, -1.26 to -0.01; P < .05). A limited number of trials were available for the effects of astaxanthin on other oxidative stress biomarkers. Astaxanthin supplementation appeared to improve superoxide dismutase activity and reduce serum isoprostane concentration in overweight subjects. Astaxanthin significantly reduced blood interleukin-6 concentration in T2DM patients (weighted mean difference: -0.70 pg/mL; 95% CI, -1.29 to -0.11 pg/mL; P = .02). The effects of astaxanthin on blood C-reactive protein and tumor necrosis factor-α concentrations were not significant. The current work indicated that astaxanthin supplementation may be beneficial for improving oxidative stress and certain inflammation biomarkers, particularly in T2DM patients. Future work should investigate the effects of astaxanthin on T2DM.
Topics: Animals; Biomarkers; Diabetes Mellitus, Type 2; Dietary Supplements; Humans; Inflammation; Oxidative Stress; Randomized Controlled Trials as Topic; Xanthophylls
PubMed: 35091276
DOI: 10.1016/j.nutres.2021.09.005 -
International Journal of Environmental... Feb 2023Several heterogeneous pathophysiology pathways have been hypothesized for being involved in the onset and course of Post-Traumatic Stress Disorder (PTSD). This... (Review)
Review
Several heterogeneous pathophysiology pathways have been hypothesized for being involved in the onset and course of Post-Traumatic Stress Disorder (PTSD). This systematic review aims to summarize the current evidence on the role of inflammation and immunological dysregulations in PTSD, investigating possible peripheral biomarkers linked to the neuroimmune response to stress. A total of 44 studies on the dysregulated inflammatory and metabolic response in subjects with PTSD with respect to controls were included. Eligibility criteria included full-text publications in the English language, human adult samples, studies involving both subjects with a clinical diagnosis of PTSD and a healthy control group. The research was focused on specific blood neuroimmune biomarkers, namely IL-1β, TNF-α, IL-6 and INF-γ, as well as on the potential harmful role of reduced antioxidant activity (involving catalase, superoxide dismutase and glutathione peroxidase). The possible role of the inflammatory-altered tryptophan metabolism was also explored. The results showed conflicting data on the role of pro-inflammatory cytokines in individuals with PTSD, and a lack of study regarding the other mediators investigated. The present research suggests the need for further studies in human samples to clarify the role of inflammation in the pathogenesis of PTSD, to define potential peripheral biomarkers.
Topics: Adult; Humans; Stress Disorders, Post-Traumatic; Cytokines; Tumor Necrosis Factor-alpha; Inflammation; Biomarkers
PubMed: 36833633
DOI: 10.3390/ijerph20042937 -
Oxidative Medicine and Cellular... 2021Oral lichen planus (OLP) is a relatively common chronic inflammatory disease of unknown etiology, which might be caused by oxidative stress and impaired antioxidant... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Oral lichen planus (OLP) is a relatively common chronic inflammatory disease of unknown etiology, which might be caused by oxidative stress and impaired antioxidant defense.
OBJECTIVE
To systematically investigate the markers of oxidative stress and antioxidant systems in the saliva and blood from OLP patients and healthy controls.
METHODS
The PubMed, Cochrane Library, and Embase were systematically queried to collect data from studies in which oxidative stress/antioxidant markers from OLP and healthy subjects had been evaluated until March 10, 2021.
RESULTS
A total of 28 studies fulfilled inclusion criteria, and 25 of them, having 849 OLP patients and 1,052 control subjects and analyzing 12 oxidative stress and antioxidant state marker levels, were subjected to meta-analysis. We found a significant decrease in total antioxidant capacity (TAC) and uric acid (UA) and a significant increase in malondialdehyde (MDA) and nitric oxide (NO) levels in the saliva and serum/plasma of OLP patients. Moreover, a significant elevation of 8-hydroxy-deoxyguanosine (8-OHdG) and advanced oxidation protein product (AOOP) level and a decrease in vitamin C were also observed in the saliva of the OLP group. In contrast, salivary vitamin A, zinc, glutathione peroxidase (GPx), vitamin E, and nitrite were not significantly different between the two groups. In single studies, markers of oxidative stresses such as superoxide dismutase (SOD) and 8-isoprostanelevels were elevated in OLP, and antioxidant parameters such as glutathione (GSH) and total protein (TP) levels were dysregulated.
CONCLUSION
This meta-analysis helps to clarify the profile of oxidative stress and antioxidant state markers in OLP patients although existing evidence is rather heterogeneous and many studies are affected by several limitations. Larger and more standardized studies are warranted to ascertain whether these markers are potential causes or effects of OLP and whether antioxidant therapy improving oxidative stress will be useful.
Topics: Adult; Aged; Antioxidants; Biomarkers; Case-Control Studies; Female; Glutathione; Glutathione Peroxidase; Humans; Lichen Planus, Oral; Male; Malondialdehyde; Middle Aged; Nitric Oxide; Oxidative Stress; Saliva; Superoxide Dismutase; Uric Acid
PubMed: 34616506
DOI: 10.1155/2021/9914652 -
Frontiers in Pharmacology 2022Accumulated experimental evidence suggests that resveratrol may have an effect on diabetic nephropathy by inhibiting inflammation and decreasing oxidative stress.... (Review)
Review
Accumulated experimental evidence suggests that resveratrol may have an effect on diabetic nephropathy by inhibiting inflammation and decreasing oxidative stress. However, the credibility of the evidence for this practice is unclear. Thus, we aimed to perform a systematic review and meta-analysis of animal studies to evaluate the antioxidant and anti-inflammatory properties of resveratrol when used in the treatment of diabetic nephropathy. Electronic bibliographic databases including PubMed, EMBASE, and Web of Science were searched for relevant studies. The methodological quality of animal studies was assessed based on the SYstematic Review Center for Laboratory animal Experimentation Risk of Bias (SYRCLE's RoB) tool. A meta-analysis was performed based on the Cochrane Handbook for Systematic Reviews of Interventions by using RevMan 5.4 software. This study was registered within International Prospective Register of Systematic Reviews (PROSPERO) as number CRD42021293784. Thirty-six qualified studies involving 726 animals were included. There was a significant association of resveratrol with the levels of blood glucose (BG), serum creatinine (Scr), blood urea nitrogen (BUN), catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), and interleukin-1β (IL-1β). Nevertheless, resveratrol treatment did not effectively decrease the levels of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, more remarkable antioxidant and hypoglycemic effects were observed in type 2 diabetic nephropathy rather than in type 1 diabetic nephropathy based on subgroup analysis. In this meta-analysis, resveratrol can exert its antioxidant activities by reducing the levels of MDA and recovering the activities of SOD, CAT, GSH, and GPx. With regard to pro-inflammatory cytokines, resveratrol had a positive effect on the reduction of IL-1β. However, the analysis indicated that resveratrol had no effect on IL-6 and TNF-α levels, probably because of the methodological quality of the studies and their heterogeneity. Current evidence supports the antioxidant and anti-inflammatory properties of resveratrol, but its relationship with the levels of some inflammatory cytokines such as IL-6 and TNF-α in animals with diabetic nephropathy needs further elucidation.
PubMed: 35355720
DOI: 10.3389/fphar.2022.841818 -
Disease Markers 2016Numerous studies suggested that oxidative stress (OS) played a central role in the onset and development of postmenopausal osteoporosis (PO); however, conflicting... (Meta-Analysis)
Meta-Analysis Review
Numerous studies suggested that oxidative stress (OS) played a central role in the onset and development of postmenopausal osteoporosis (PO); however, conflicting results were obtained as to the association of OS-related biomarkers and PO. This meta-analysis aimed to identify the association between these markers and PO, and explore factors that may explain the inconsistencies in these results. A systematic literature search was conducted in relevant database. Search terms and selection criteria were priorly determined to identify and include all studies that detected markers of OS in PO patients. We pooled data with a random effects meta-analysis with standardized mean differences and 95% confidence interval. Total 17 studies including 12 OS markers were adopted. The results showed that superoxide dismutase (SOD) in erythrocytes, catalase (CAT), total antioxidant status (TAS), hydroperoxides (HY), advanced oxidation protein products (AOPP), malondialdehyde (MDA), and vitamin B12 (VB12) in plasma/serum were not statistically different between the PO and control group, whereas significantly increased level of homocysteine (Hcy) and nitric oxide (NO), along with decreased SOD, glutathione peroxidase (GPx), folate, and total antioxidant power (TAP) in plasma/serum were obtained in the PO group. In summary, OS might serve as potential biomarkers in the etiopathophysiology and clinical course of PO.
Topics: Biomarkers; Female; Humans; Osteoporosis, Postmenopausal; Oxidative Stress
PubMed: 27594735
DOI: 10.1155/2016/7067984 -
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 -
Journal of Dentistry Jul 2024To analyze the role of oxidative stress (OS) biomarkers in peri‑implant diseases using a systematic review and meta-analysis approach. DATE: The review incorporated... (Meta-Analysis)
Meta-Analysis Review
OBJECTIVES
To analyze the role of oxidative stress (OS) biomarkers in peri‑implant diseases using a systematic review and meta-analysis approach. DATE: The review incorporated cross-sectional studies, randomized controlled trials, and case-control trials to evaluate the differences in OS biomarkers of peri‑implant disease.
SOURCES
A comprehensive literature search was conducted in electronic databases such as PubMed, Scopus, Embase, Web of Science, and CNKI, and no restrictions were applied during the search process.
STUDY SELECTION
A total of 452 studies were identified, of which 18 were eligible for inclusion. Risk of bias and sensitivity analysis were assessed using Egger's test and funnel plots.
RESULTS
We found that the levels of glutathione peroxidase (GSH-Px) in the peri‑implant sulcus fluid (PISF) of patients with peri‑implant diseases were significantly reduced (SMD = -1.40; 95 % CI = 1.70, -1.11; p < 0.001), while the levels of total myeloperoxidase (MPO) and malondialdehyde (MDA) were significantly increased (SMD = 0.46; 95 % CI = 0.12, 0.80; p = 0.008; SMD = 0.28; 95 % CI = 0.01, 0.56; p = 0.043). However, there were no significant differences of MPO concentration (SMD = 0.38; 95 % CI = -0.39, 1.15; p = 0.331) and superoxide dismutase (SOD)(SMD = -0.43; 95 % CI = -1.94, 1.07; p = 0.572) in PISF between peri‑implant disease group and control group. Similarly, salivary MPO did not show significant differences (SMD = 1.62; 95 % CI = -1.01, 4.24; p = 0.227).
CONCLUSIONS
Our results supported that the level of local OS biomarkers was closely related to peri‑implant diseases. GSH-Px, total MPO and MDA may be PISF biomarkers with good capability to monitor the development of peri‑implant disease.
CLINICAL SIGNIFICANCE
This study found significant differences in the levels of local OS biomarkers (GSH-Px, total MPO, and MDA) between patients with peri‑implant diseases and healthy subjects, which may be ideal candidate biomarkers for predicting and diagnosing peri‑implant diseases.
Topics: Humans; Oxidative Stress; Biomarkers; Peroxidase; Malondialdehyde; Peri-Implantitis; Glutathione Peroxidase; Dental Implants; Gingival Crevicular Fluid
PubMed: 38679134
DOI: 10.1016/j.jdent.2024.105026