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ACS Nano Apr 2024Substantial advancements have been achieved in the realm of cardiac tissue repair utilizing functional hydrogel materials. Additionally, drug-loaded hydrogels have...
Substantial advancements have been achieved in the realm of cardiac tissue repair utilizing functional hydrogel materials. Additionally, drug-loaded hydrogels have emerged as a research hotspot for modulating adverse microenvironments and preventing left ventricular remodeling after myocardial infarction (MI), thereby fostering improved reparative outcomes. In this study, diacrylated Pluronic F127 micelles were used as macro-cross-linkers for the hydrogel, and the hydrophobic drug α-tocopherol (α-TOH) was loaded. Through the synthesis of polydopamine (PDA) and the incorporation of conductive components, an injectable and highly compliant antioxidant/conductive composite FPDA hydrogel was constructed. The hydrogel exhibited exceptional stretchability, high toughness, good conductivity, cell affinity, and tissue adhesion. In a rabbit model, the material was surgically implanted onto the myocardial tissue, subsequent to the ligation of the left anterior descending coronary artery. Four weeks postimplantation, there was discernible functional recovery, manifesting as augmented fractional shortening and ejection fraction, alongside reduced infarcted areas. The findings of this investigation underscore the substantial utility of FPDA hydrogels given their proactive capacity to modulate the post-MI infarct microenvironment and thereby enhance the therapeutic outcomes of myocardial infarction.
Topics: Animals; Rabbits; Hydrogels; alpha-Tocopherol; Myocardial Infarction; Myocardium; Ventricular Remodeling
PubMed: 38436241
DOI: 10.1021/acsnano.4c00509 -
The British Journal of Nutrition Dec 2023Childhood is a critical period for muscle accumulation. Studies in elders have reported that antioxidant vitamins could improve muscle health. However, limited studies...
Childhood is a critical period for muscle accumulation. Studies in elders have reported that antioxidant vitamins could improve muscle health. However, limited studies have assessed such associations in children. This study included 243 boys and 183 girls. A seventy-nine-item FFQ was used to investigate dietary nutrients intake. Plasma levels of retinol and -tocopherol were measured using high-performance liquid chromatography with MS. Dual X-ray absorptiometry was used to assess appendicular skeletal muscle mass (ASM) and total body fat. The ASM index (ASMI) and ASMI Z-score were then calculated. Hand grip strength was measured using a Jamar® Plus+ Hand Dynamometer. Fully adjusted multiple linear regression models showed that for each unit increase in plasma retinol content, ASM, ASMI, left HGS and ASMI Z-score increased by 2·43 × 10 kg, 1·33 × 10 kg/m, 3·72 × 10 kg and 2·45 × 10 in girls, respectively ( < 0·001-0·050). ANCOVA revealed a dose-response relationship between tertiles of plasma retinol level and muscle indicators (: 0·001-0·007). The percentage differences between the top and bottom tertiles were 8·38 %, 6·26 %, 13·2 %, 12·1 % and 116 % for ASM, ASMI, left HGS, right HGS and ASMI Z-score in girls, respectively (: 0·005-0·020). No such associations were observed in boys. Plasma -tocopherol levels were not correlated with muscle indicators in either sex. In conclusion, high circulating retinol levels are positively associated with muscle mass and strength in school-age girls.
Topics: Male; Female; Child; Humans; Aged; Vitamin A; alpha-Tocopherol; Hand Strength; Muscle, Skeletal; Absorptiometry, Photon; China; Sarcopenia
PubMed: 37341020
DOI: 10.1017/S0007114523001265 -
Journal of Bone and Mineral Metabolism Jul 2023To analyze the association between α-tocopherol intake and cadmium (Cd) exposure and osteoporosis in population ≥ 50 years.
INTRODUCTION
To analyze the association between α-tocopherol intake and cadmium (Cd) exposure and osteoporosis in population ≥ 50 years.
MATERIALS AND METHODS
Sociodemographic data, physical examination, and laboratory indicators including serum Cd level and dietary α-tocopherol intake of 8459 participants were extracted from the National Health and Nutrition Examination Survey (NHANES) database in this cross-sectional study. The associations between α-tocopherol intake, serum Cd levels and osteoporosis were evaluated using univariate and multivariate logistic regression analyses, with the estimated value (β), odds ratios (ORs) and 95% confidence intervals (CIs). We further explored the impact of α-tocopherol intake on Cd exposure and the bone mineral density (BMD) in total femur and femur neck.
RESULTS
A total of 543 old adults suffered from osteoporosis. The serum Cd level (0.52 μg/L vs. 0.37 μg/L) and α-tocopherol intake (5.28 mg vs. 6.50 mg) were statistical different in osteoporosis group and non-osteoporosis group, respectively. High level of Cd exposure was related to the increased risk of osteoporosis [OR = 1.60, 95% CI (1.15-2.21)]. In the total femur, α-tocopherol intake may improve the loss of BMD that associated with Cd exposure [β = - 0.047, P = 0.037]. Moreover, high α-tocopherol intake combined with low Cd exposure [OR = 0.54, 95% CI (0.36-0.81)] was linked to the decreased risk of osteoporosis comparing with low α-tocopherol intake combined with high Cd exposure.
CONCLUSION
High α-tocopherol intake may improve the Cd-related osteoporosis and loss of BMD that could provide some dietary reference for prevention of osteoporosis in population ≥ 50 years old.
Topics: Adult; Humans; Middle Aged; alpha-Tocopherol; Cadmium; Nutrition Surveys; Cross-Sectional Studies; Osteoporosis; Bone Density; Eating
PubMed: 37036532
DOI: 10.1007/s00774-023-01418-x -
Food & Function Jan 2024Minor constituents exhibit certain antioxidant interactions , and the effects in different media are different. However, it is not clear whether there are antioxidant...
Minor constituents exhibit certain antioxidant interactions , and the effects in different media are different. However, it is not clear whether there are antioxidant interactions in cells after digestion and absorption. We utilized the cellular antioxidant evaluation model in HepG2 cells to study the antioxidant interaction between α-tocopherol and γ-oryzanol, and the interaction mechanism of a binary mixture was also illustrated. A cellular antioxidant assay (CAA) model and a combined index (CI) method were firstly used to explore the antioxidant activity and interaction of the binary mixture in HepG2 cells. The CAA value was positively correlated with the single addition concentration, while the results displayed a biphasic tendency with increasing concentrations of the binary mixture. The combination of TO11 (1 μg mL α-tocopherol and 10 μg mL γ-oryzanol) showed the greatest antioxidant activity and synergistic effect, and the maximum CAA value reached up to 94.84 ± 4.2. Then the mechanism of the synergistic antioxidant effect of the binary mixture was explained from three aspects including cellular uptake, intracellular reactive oxygen species (ROS) level and endogenous enzyme activity. The results demonstrated that the antioxidant interaction of the binary mixture in cells was related to cellular uptake of minor constituents, and the combination of TO11 exerted a synergistic effect by scavenging ROS and up-regulating glutathione peroxidase (GSH-Px) activity, resulting in the strongest cellular antioxidant activity. This study throws light on the nature of antioxidant interaction between minor constituents, which may contribute to the development of related functional foods and rational dietary collocation.
Topics: Humans; Antioxidants; alpha-Tocopherol; Reactive Oxygen Species; Hep G2 Cells; Phenylpropionates
PubMed: 38179649
DOI: 10.1039/d3fo03727d -
International Journal of Molecular... Jul 2023With the advancement of in vivo studies and clinical trials, the pathogenesis of neurodegenerative diseases has been better understood. However, gaps still need to be... (Review)
Review
With the advancement of in vivo studies and clinical trials, the pathogenesis of neurodegenerative diseases has been better understood. However, gaps still need to be better elucidated, which justifies the publication of reviews that explore the mechanisms related to the development of these diseases. Studies show that vitamin E supplementation can protect neurons from the damage caused by oxidative stress, with a positive impact on the prevention and progression of neurodegenerative diseases. Thus, this review aims to summarize the scientific evidence of the effects of vitamin E supplementation on neuroprotection and on neurodegeneration markers in experimental models. A search for studies published between 2000 and 2023 was carried out in the PubMed, Web of Science, Virtual Health Library (BVS), and Embase databases, in which the effects of vitamin E in experimental models of neurodegeneration were investigated. A total of 5669 potentially eligible studies were identified. After excluding the duplicates, 5373 remained, of which 5253 were excluded after checking the titles, 90 articles after reading the abstracts, and 11 after fully reviewing the manuscripts, leaving 19 publications to be included in this review. Experiments with in vivo models of neurodegenerative diseases demonstrated that vitamin E supplementation significantly improved memory, cognition, learning, motor function, and brain markers associated with neuroregeneration and neuroprotection. Vitamin E supplementation reduced beta-amyloid (Aβ) deposition and toxicity in experimental models of Alzheimer's disease. In addition, it decreased tau-protein hyperphosphorylation and increased superoxide dismutase and brain-derived neurotrophic factor (BDNF) levels in rodents, which seems to indicate the potential use of vitamin E in preventing and delaying the progress of degenerative lesions in the central nervous system.
Topics: Humans; Vitamin E; Neurodegenerative Diseases; Alzheimer Disease; Cognition; Models, Theoretical
PubMed: 37446369
DOI: 10.3390/ijms241311191 -
JAMA Network Open Aug 2023Research suggests that increased mitochondrial DNA copy number (mtDNAcn) is associated with increased risk of non-Hodgkin lymphoma (NHL); however, no studies to date...
IMPORTANCE
Research suggests that increased mitochondrial DNA copy number (mtDNAcn) is associated with increased risk of non-Hodgkin lymphoma (NHL); however, no studies to date have evaluated whether the mitochondrial DNA fraction with breaks (mtDNAfb) is associated with risk of NHL.
OBJECTIVE
To evaluate the association of mtDNAfb with NHL risk.
DESIGN, SETTING, AND PARTICIPANTS
This nested case-control study, which used prospectively collected samples as part of baseline enrollment (from 1985 through 1988) of 29 133 men who smoked for the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) Study conducted in southwest Finland, included 107 incident NHL cases and 107 controls (matched on date of birth ±5 years). Analyses were conducted from January to September 2022.
EXPOSURE
High-throughput real-time polymerase chain reaction assays quantifying mtDNAfb.
MAIN OUTCOMES AND MEASURES
Incident NHL cases were identified in the ATBC Study through April 30, 2002, using the Finnish Cancer Registry and the Register of Causes of Death. The mtDNAfb was quantified and categorized based on the median, tertile, and quartile distributions among controls. Odds ratios (ORs) and 95% CIs were estimated using conditional logistic regression models to assess the associations between categorized mtDNAfb and future risk of NHL, controlling for age, body mass index, number of cigarettes smoked per day, number of pack-years, and mtDNAcn.
RESULTS
A total of 29 133 men (median [IQR] age, 57.2 [52.6-62.5] years) participated in ATBC Study. Higher mtDNAfb was associated with an increased risk of NHL (median OR, 2.89; 95% CI, 1.40-5.93) in a dose-dependent manner (quartile 2 vs 1 OR, 1.24; 95% CI, 0.43-3.40; quartile 3 vs 1 OR, 3.58; 95% CI, 1.39-9.24; quartile 4 vs 1 OR, 3.42; 95% CI, 1.30- 8.99; P = .004 for trend).
CONCLUSIONS AND RELEVANCE
This study's findings suggest that increased mtDNAfb is associated with an increased future risk of NHL. Additional studies are needed to confirm these findings, particularly among women and nonsmokers.
Topics: Male; Humans; Female; Middle Aged; DNA, Mitochondrial; Risk Factors; Case-Control Studies; DNA Fragmentation; Lymphoma, Non-Hodgkin
PubMed: 37531109
DOI: 10.1001/jamanetworkopen.2023.26885 -
Gastric Cancer : Official Journal of... Nov 2023Obesity has been positively associated with gastric cancer. Excess fat impacts hormones, which have been implicated in carcinogenesis. We investigated obesity-related...
BACKGROUND
Obesity has been positively associated with gastric cancer. Excess fat impacts hormones, which have been implicated in carcinogenesis. We investigated obesity-related hormones and cardia gastric cancer (CGC) and non-cardia gastric cancer (NCGC) risk.
METHODS
Nested case-control studies were conducted within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort (61 CGCs, and 172 NCGCs and matched controls) and the Alpha-Tocopherol, Beta-Carotene Cancer Prevention (ATBC) study (100 CGCs and 65 NCGCs and matched controls); serum hormones were measured. In UK-Biobank (n = 458,713), we included 137 CGCs and 92 NCGCs. Sex-specific analyses were conducted. For EPIC and ATBC, odds ratios (ORs), and for UK-Biobank hazard ratios (HRs), were estimated using conditional logistic regression and Cox regression, respectively.
RESULTS
Insulin-like growth-factor-1 was positively associated with CGC and NCGC in EPIC men (OR 1.94, 95% CI 1.03-3.63; OR 1.63, 95% CI 1.05-2.53, respectively), with similar findings for CGC in UK-Biobank women (HR 1.76, 95% CI 1.08-2.88). Leptin in EPIC men and C-peptide in EPIC women were positively associated with NCGC (OR 2.72, 95% CI 1.01-7.34 and OR 2.17, 95% CI 1.19-3.97, respectively). Sex hormone-binding globulin was positively associated with CGC in UK-Biobank men (HR 1.29, 95% CI 1.02-1.64). Conversely, ghrelin was inversely associated with NCGC among EPIC and ATBC men (OR 0.53, 95% CI 0.34-0.84; OR 0.22, 95% CI 0.10-0.50, respectively). In addition, dehydroepiandrosterone was inversely associated with CGC in EPIC and ATBC men combined.
CONCLUSIONS
Some obesity-related hormones influence CGC and NCGC risk.
Topics: Male; Humans; Female; Stomach Neoplasms; Prospective Studies; Cohort Studies; Obesity; Logistic Models; Hormones
PubMed: 37455285
DOI: 10.1007/s10120-023-01414-0 -
Journal of Trace Elements in Medicine... Dec 2023Lead impairs female reproductive health because it can induce oxidative stress. Zinc as an antioxidant produces an enzyme system that helps neutralize free radicals....
BACKGROUND
Lead impairs female reproductive health because it can induce oxidative stress. Zinc as an antioxidant produces an enzyme system that helps neutralize free radicals. α-Tocopherol has an antagonistic effect that reduces oxidative stress. This study aimed to demonstrate the effects of zinc (Zn) and α-tocopherol on the ovarian endogenous antioxidants and antral follicles of albino rats (Rattus norvegicus) exposed to lead acetate (Pb(CHO)).
METHODS
Twenty-five female Wistar rats were divided into five groups, namely groups K (control), P0, P1, P2, and P3. Following exposure and treatment for 21 days with different combinations, the albino rats were necropsied, and their ovaries were removed for subsequent histopathological preparations and endogenous antioxidant analysis. Observations were made on the ovary, including an antral follicle count and diameter calculations. Analysis of the superoxide dismutase (SOD) levels (560 nm wavelength) and malondialdehyde MDA-TBA (532 nm wavelength) were performed by a spectrophotometer. The data were analyzed using a one-way ANOVA and least significant difference (LSD) test with the SPSS V24 software.
RESULTS
The highest SOD enzyme expression in the albino rat ovaries was in P0 (17.23 ± 5.34), and the lowest was in P3 (4.21 ± 0.76). The lowest MDA level was observed in the control group (K) and P3 compared to the other groups. The highest average antral follicle count and diameter were found in the albino rats exposed to 1.5 mg/kg BW lead acetate, and treated with 0.54 mg/kg BW zinc sulfate and 100 mg/kg BW α-tocopherol (group P3) compared to the other groups. The mechanisms of action of zinc and α-tocopherol work synergistically to decrease free radicals and ovarian damage.
CONCLUSION
The results showed that a combination of 0.54 mg/kg BW zinc (Zn) and 100 mg/kg BW α-tocopherol can maintain the number and diameter of the antral follicles and reduce ovarian SOD expression and MDA levels in albino rats exposed to lead acetate.
Topics: Rats; Female; Animals; Antioxidants; alpha-Tocopherol; Lead; Zinc; Rats, Wistar; Oxidative Stress; Superoxide Dismutase; Free Radicals; Acetates
PubMed: 37657266
DOI: 10.1016/j.jtemb.2023.127284 -
Advanced Science (Weinheim,... Oct 2023Topical chemotherapy approaches are relevant for certain skin cancer treatments. This study observes that cabazitaxel (CTX), a broad-spectrum second-generation taxane...
Topical chemotherapy approaches are relevant for certain skin cancer treatments. This study observes that cabazitaxel (CTX), a broad-spectrum second-generation taxane cytotoxic agent, can be dissolved in α-tocopherol at high concentrations exceeding 100 mg mL . 2D nuclear magnetic resonance (NMR) analysis and molecular dynamics (MD) are used to study this phenomenon. The addition of 30% dimethyl sulfoxide (DMSO) to the α-tocopherol/CTX solution improves its working viscosity and enhances CTX permeation through human skin in vitro (over 5 µg cm within 24 h), while no detectable drug permeates when CTX is dissolved in α-tocopherol alone. In a transepidermal water loss assay, the barrier impairment induced by CTX in 30% DMSO in α-tocopherol, but not in pure DMSO, is reversible 8 h after the formulation removal from the skin surface. Antitumor efficacy of the topical CTX formulation is evaluated in nude mice bearing A431 human squamous carcinoma skin cancer xenografts. With topical application of concentrated CTX solutions (75 mg mL ), tumor growth is significantly suppressed compared to lower concentration groups (0, 25, or 50 mg mL CTX). Taken together, these findings show that topical delivery of CTX using a DMSO and α-tocopherol solvent warrants further study as a treatment for skin malignancies.
Topics: Mice; Animals; Humans; alpha-Tocopherol; Dimethyl Sulfoxide; Mice, Nude; Taxoids; Skin Neoplasms
PubMed: 37555802
DOI: 10.1002/advs.202302658 -
Journal of Clinical Periodontology Nov 2023To evaluate whether and how gut microbiota-meditated metabolites regulate alveolar bone homeostasis in diabetic periodontitis (DP).
AIM
To evaluate whether and how gut microbiota-meditated metabolites regulate alveolar bone homeostasis in diabetic periodontitis (DP).
MATERIALS AND METHODS
Lactobacillus casei (L. casei) was employed as a positive modulator of gut microbiota in DP mice. The destruction of alveolar bone was evaluated. Untargeted metabolomics was conducted to screen out the pivotal metabolites. A co-housing experiment was conducted to determine the connection between the gut microbiota and alpha-tocopherol acetate (α-TA). α-TA was applied to DP mice to investigate its effect against alveolar bone loss. Human periodontal ligament cells (hPDLCs) and human gingival fibroblasts (HGFs) were extracted for the in vitro experiment. Transcriptomic analysis and immunohistochemistry were performed to detect the major affected signalling pathways.
RESULTS
Positive regulation of the gut microbiota significantly attenuated alveolar bone loss and increased the serum α-TA level. The alteration in gut microbiota composition could affect the serum α-T (the hydrolysates of α-TA) level. α-TA could alleviate alveolar bone destruction in DP mice and α-T exert beneficial effects on hPDLCs and HGFs. Mechanistically, the STAT3 signalling pathway was the pivotal pathway involved in the protective role of α-TA.
CONCLUSIONS
The gut microbiota-α-TA-STAT3 axis plays an important role in the regulation of diabetic alveolar bone homeostasis.
Topics: Mice; Humans; Animals; Alveolar Bone Loss; alpha-Tocopherol; Gastrointestinal Microbiome; Periodontitis; Diabetes Mellitus; STAT3 Transcription Factor
PubMed: 37596824
DOI: 10.1111/jcpe.13862