Although numerous clinical studies suggest that ginseng supplementation may benefit cardiovascular disease (CVD) risk factors, results remain inconclusive. This systematic review and meta-analysis evaluated the effects of ginseng supplementation on CVD-related risk factors. Relevant studies were identified through electronic searches in Embase, Web of Science, Scopus, PubMed, and CENTRAL up to August 2024. Statistical analyses, including a random-effects model, meta-regression, and non-linear modeling, were used to assess heterogeneity, dose-response relationships, and the overall effects of ginseng supplementation. A total of 70 studies, published between 1998 and 2024 and involving 4,506 participants, were included. Ginseng supplementation significantly affected several biochemical markers, including high-sensitivity C-reactive protein (hs-CRP) (SMD: -0.23; 95% CI: -0.38, -0.08; P = 0.002), gamma-glutamyl transferase (GGT) (SMD: -0.20; 95% CI: -0.36, -0.04; P = 0.015), glutathione reductase (GSH-Rd) (SMD: 0.90; 95% CI: 0.38, 1.42; P = 0.001), reactive oxygen species (ROS) (SMD: -0.94; 95% CI: -1.27, -0.60; P < 0.001), and superoxide dismutase (SOD) (SMD: 0.48; 95% CI: 0.10, 0.87; P = 0.014). Meta-regression analysis showed significant linear associations between ginseng dosage and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) (P = 0.044), and between supplementation duration and malondialdehyde (MDA) (P = 0.007). Dose-response analysis revealed significant associations between ginseng dose and fasting blood glucose (FBG) (P < 0.001), hs-CRP (P = 0.043), Interleukin-6 (IL-6) (P = 0.041), diastolic blood pressure (DBP) (P = 0.022), Interleukin-10 (IL-10) (P = 0.048), fasting insulin (P = 0.012), and total protein (P = 0.010). Supplementation duration was positively associated with MDA levels (P = 0.008). Ginseng supplementation was associated with improvements in inflammatory markers, liver function, and oxidative stress parameters. No significant effects were observed on anthropometric indices, blood pressure, glycemic profile, lipid profile, adipokines, or heart rate.

The objective was to evaluate the use of resveratrol conjugated with silica nanoparticles during the in vitro maturation of bovine oocytes. The oocytes were divided into the following treatment groups during the maturation process: control (n = 159), resveratrol 0.5 μM (n = 158), resveratrol 1 μM (n = 155), nanoparticles conjugated with 0.5 μM resveratrol (n = 159), and nanoparticles conjugated with 1 μM resveratrol (n = 158). Several parameters were assessed, including cumulus oophorus size, reactive oxygen species (ROS) production, oocyte nuclear maturation, cell apoptosis, cleavage rates, and blastocyst production rates. Statistical analysis was conducted using Sigma Plot software (version 11) and SAS Studio, with statistical significance defined as P ≤ 0.05 for the main effects and interactions. The results indicated that the cumulus oophorus size was smaller in the resveratrol 1 μM treatment group, and the oocyte size was reduced in the nanoparticle 1 μM treatment group. No significant differences were detected between the treatment groups in terms of ROS production, oocyte maturation, or cell apoptosis. However, the resveratrol 1 μM treatment group exhibited decreased rates of cleavage and blastocyst formation. In contrast, the nanoparticles 0.5 μM and 1.0 μM treatments showed improved cleavage and blastocyst rates compared with the resveratrol 1.0 μM treatment group. In summary, while resveratrol alone at 1 μM concentration had a negative impact on cleavage and blastocyst rates, the use of silica nanoparticles conjugated with resveratrol (both 0.5 μM and 1 μM) enhanced these outcomes, suggesting a potential advantage in using nanoparticle-conjugated resveratrol for the in vitro maturation of bovine oocytes.

The extracellular matrices, such as the haemolymph, in insects are at the centre of most physiological processes and are protected from oxidative stress by the extracellular antioxidant enzymes. In this study, we identified two secreted superoxide dismutase genes (PxSOD3 and PxSOD5) and investigated the oxidative stress induced by chlorpyrifos (CPF) in the aquatic insect Protohermes xanthodes (Megaloptera: Corydalidae). PxSOD3 and PxSOD5 contain the signal peptides at the N-terminus. Structure analysis revealed that PxSOD3 and PxSOD5 contain the conserved CuZn-SOD domain, which is mainly composed of β-sheets and has conserved copper and zinc binding sites. Both PxSOD3 and PxSOD5 are predicted to be soluble proteins located in the extracellular space. After exposure to different concentrations of sublethal CPF, MDA content in P. xanthodes larvae were increased in a dose-dependent manner; SOD and CAT activities were also higher in CPF-treated groups than that in the no CPF control, indicating that sublethal CPF induces oxidative stress in P. xanthodes larvae. Furthermore, PxSOD3 and PxSOD5 expression levels and haemolymph SOD activity in the larvae were downregulated by sublethal CPF at different concentrations. Our results suggest that the PxSOD3 and PxSOD5 are putative extracellular antioxidant enzymes that may play a role in maintaining the oxidative balance in the extracellular space. Sublethal CPF may induce oxidative stress in the extracellular space of P. xanthodes by reducing the gene expression and catalytic activity of extracellular SODs.

This study aimed to evaluate the effects of acetyl-L-carnitine on follicle survival and growth, stromal cell density and extracellular matrix, as well as on the expression of mRNA for nuclear factor erythroid 2-related factor (NRF2), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX) and peroxiredoxin 6 (PRDX6) in cultured bovine ovarian cortical tissues. Ovarian fragments (3 × 3 × 1 mm) were cultured for 6 days in α-MEM+ alone or supplemented with 10, 50 or 100 μM acetyl-L-carnitine at 38.5°C with 5% CO2 in humidified air. Before (non-cultured tissues) and after culture, the ovarian fragments were fixed in 4% paraformaldehyde for 12 h for histological analysis or stored at –80ºC for mRNA expression analysis of NRF2, SOD, CAT, PRDX6 and GPX1. The results showed that 100 μM acetyl-L-carnitine increased the percentages of morphologically normal follicles and stromal cell density in cultured ovarian tissues. On the other hand, acetyl-L-carnitine did not influence the percentage of collagen in ovarian tissue nor the expression of mRNAs for NRF2, SOD, CAT, PRDX6 and GPX1. In conclusion, 100 μM acetyl-L-carnitine increased follicle survival and stromal cell density in cultured bovine ovarian tissues but does not influence collagen fibre distribution or the expression of mRNAs for NRF2, SOD, CAT, PRDX6 and GPX1.

Thyroid disorders are increasingly prevalent globally and are considered metabolic-lifestyle diseases. While medications can manage thyroid dysfunction, they are usually lifelong, costly and not always practical. Intermittent fasting (IF), a highly adaptable dietary regimen, has been shown to influence lifestyle, gut microbiome and circadian rhythms. Our study hypothesised that IF, combined with vitamin supplementation, could reduce the risk of thyroid disorders due to their antioxidant effects. In this study, experimental animals were divided into five groups: euthyroid, hypothyroidism control, IF + vitamin E (Vit. E), Vit. E and IF. Hypothyroidism was induced using propylthiouracil over 24 days, and IF and Vit. E (66 mg/ml) were administered based on the experimental group. The hypothyroid animals exhibited increased anxiety, weight gain, lipid peroxidation and a significant reduction in thyroid hormone levels, locomotor activity and antioxidant levels—clear signs of thyroid dysfunction’s impact on metabolism and overall health. Our proposed therapies IF and Vit. E effectively mitigated thyroid damage. Drawing inspiration from ancient ayurveda and modern healthcare strategies, these cost-effective and practical regimens offer a promising solution to managing thyroid disorders globally.

Inflammation and oxidative stress contribute to the progression of chronic diseases, and the volume of research in this area is rapidly expanding. Various dietary indices have been developed to determine the overall inflammatory or oxidative stress potential of a diet; however, few have been validated in cardiometabolic disease populations. This review aimed to explore the association between dietary indices and biomarkers of inflammation and oxidative stress in adults with cardiometabolic conditions. Four databases were systematically searched for literature in any language (Embase, CINAHL, CENTRAL and MEDLINE) with 12,286 deduplicated records identified. Seventeen studies of adults with metabolic syndrome, cardiovascular disease, type 2 diabetes, non-alcoholic fatty liver disease or chronic kidney disease were included. Fourteen studies were observational studies, one study was a clinical trial, and one was a randomised controlled trial. Four dietary indices were reported on with most studies (n 11) reporting on the dietary inflammatory index. The most reported biomarker was C-reactive protein. The findings were narratively synthesised. Results were inconclusive due to the heterogeneity of dietary indices and their use, disease states and biomarkers reported. Only one study reporting on the dietary inflammatory index assessed all 45 parameters. Observational studies, particularly retrospective designs (n 7), are subject to recall and selection biases, potentially presenting overestimated results. Further research is required to determine the relationship between dietary indices and biomarkers of inflammation and oxidative stress in cardiometabolic disease populations. Future research should be prospective, utilise rigorous research methods, assess the full range of index parameters, and examine biomarkers the tool was developed for.

Green tea, a plant rich in bioactive compounds, has been highlighted for its beneficial effects. In the present systematic review and meta-analysis of randomised controlled trials (RCTs), the impact of green tea on inflammatory and oxidative markers is investigated. Using pre-defined keywords, online databases (PubMed, Scopus, Web of Science Core Collection, and Google Scholar) were searched for relevant articles, published from inception up to February 2024. The outcomes included C-reactive protein (CRP), tumour necrosis factor-α (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), total antioxidant capacity (TAC), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPX). Analyses of subgroups, linear, and non-linear associations were also carried out. Out of 1264 records initially retrieved, 38 RCTs were included. Supplementation with green tea improved the following indicators: IL-1β (weighted mean difference (WMD): −0.10 pg/mL; 95% CI: −0.15, -0.06), MDA (WMD: −0.40 mcmol/L; 95 % CI: −0.63, −0.18), TAC (WMD: 0.09 mmol/L; 95% CI: 0.05, 0.13), SOD (WMD: 17.21 u/L; 95% CI: 3.24, 31.19), and GPX (WMD: 3.90 u/L; 95% CI: 1.85, 5.95); but failed to improve others, including CRP (WMD: 0.01 mg/L; 95% CI: −0.14, 0.15), IL-6 (WMD: −0.34 pg/mL; 95% CI:−0.94, 0.26), and TNF-α (WMD: −0.07 pg/mL; 95% CI: −0.42, 0.28). Supplementation with green tea can improve the body’s oxidative status. However, the results showed no significant effect of green tea on inflammatory markers, except for IL-1β. Further studies are needed to determine the effectiveness of green tea, particularly on inflammatory status.

The primary causes of female mortality often involve diseases related to oxidative stress. Dietary total antioxidant capacity (TAC) evaluates its antioxidant content and potential health effects. This study, registered with PROSPERO (ID: CRD42024427784), explores the association between dietary TAC and women’s health outcomes, including endocrine conditions with gynaecological implications, obstetric outcomes, gynaecological conditions and oncological diseases related to the female reproductive system. We conducted a systematic search in MEDLINE (via PubMed), EMBASE, LILACS and CINAHL for observational studies published up to February 2024 that explored the relationship between dietary TAC and these health conditions. Data were analysed using RevMan 5·4 software. Nineteen studies met the eligibility criteria (sample sizes: 64–3209 women) and examined various conditions, including neoplasms (breast, endometrial and ovarian), bacterial vaginosis, menopause, polycystic ovary syndrome (PCOS), pre-eclampsia (PE), gestational diabetes mellitus (GDM), miscarriage, infertility and inflammation and oxidative stress markers. The meta-analysis identified a significant association between dietary TAC, measured in vitamin C equivalents, and breast cancer, revealing that women with the disease had a lower dietary TAC due to reduced antioxidant intake. Mixed results were found for endometrial cancer, while higher TAC levels were associated with a lower risk of PCOS and infertility. Among postmenopausal women, higher TAC correlated with fewer symptoms such as sleep issues and anxiety. In gestational conditions, higher dietary TAC was linked to a lower risk of miscarriage, GDM and PE. Twelve of the nineteen studies demonstrated significant associations between dietary TAC and the outcomes of interest.

Current evidence points to a research-practice gap in mental health. There is a specific unmet need to identify novel strategies to improve diagnostic criteria, especially when clinical manifestations overlap as in the case of bipolar (BD) and major depressive disorder (MDD). Based on the rapidly evolving notion that affective disorders are characterized by disrupted brain-body communication, current efforts of neuropsychiatric research are converging towards the identification of specific clusters of peripheral interconnected biomarkers. We argue that these can capture the complexity of the disease as they are linked to the fundamental pathophysiological mechanisms underlying BD or MDD, and can thus deliver an unbiased biosignature. Here we provide a critical viewpoint on the promises and challenges of biomarkers to identify reliable biosignatures of affective disorders. Novel methodological insight and relevant biomarkers are discussed with a main focus on immunometabolic derangements and disrupted redox balance. Major advancements are reviewed taking into consideration that an unbiased diagnosis can only derive from a deep understanding of how biological, psychological, and social factors interact ultimately affecting the clinical manifestation of affective disorders.

The therapeutic effects of probiotics in patients with traumatic brain injury (TBI) remain unclear. This study aimed to investigate the effects of probiotic supplementation on cell adhesion molecules (CAMs), oxidative stress and antioxidant parameters in TBI patients. This randomised, double-blind, placebo-controlled trial included forty-six TBI patients who were randomly assigned to receive either a probiotic supplement (n 23) or a placebo (n 23) for 14 d. The probiotic capsule contained four strains of Lactobacillus (L. casei, L. bulgaricus, L. rhamnosus, L. acidophilus), two strains of Bifidobacterium (B. longum, B. breve) and Streptococcus thermophilus. Serum levels of intercellular adhesion molecule (ICAM)-1, vascular cell adhesion molecule (VCAM)-1, pro-oxidant–antioxidant balance (PAB), malondialdehyde (MDA), nitric oxide (NO), total antioxidant capacity (TAC) and arylesterase (ARE) activity were measured at the beginning and end of the trial. Dietary intakes of patients were also recorded at the beginning and end of the trial. At the end of the study, there were no significant changes in ICAM-1, VCAM-1, PAB, MDA, NO, TAC and ARE levels. However, patients who received probiotic supplements had significantly increased dietary intakes of energy, macronutrients, vitamin E, Zn, Cu and Se compared with the placebo group. This study provides evidence that probiotic supplementation for 14 d in TBI patients has beneficial effects on dietary intake. However, it did not affect serum levels of CAMs, oxidative stress or antioxidant parameters. These findings should be considered preliminary, and further research is needed to evaluate long-term and clinical outcomes.

Trichinellosis is a widespread food-borne zoonosis, causing mild to severe illness in humans with potential fatality. Its treatment remains challenging due to the side effects and limited efficacy of specific drugs. Therefore, the current study was conducted to assess the therapeutic effects of ellagic acid (EA) alone and combined with albendazole against trichinellosis and its biochemical and pathological alterations in mice. Mice were divided into two main groups: G1 and G2 for the intestinal and muscular phases, respectively. Then each group was subdivided into five subgroups: (a) non-infected control, (b) infected control non-treated, (c) infected and treated with EA, (d) infected and treated with albendazole, and (e) infected and treated with a combination of both. Parasitological, biochemical, and histopathological studies were used to evaluate the therapeutic outcomes. Treatment with EA resulted in a significant reduction of the mean counts of intestinal adult worms and muscular larvae compared to the infected control. EA improved oxidative stress as it reduced nitric oxide and increased catalase activities in intestinal and muscular tissues. Additionally, it alleviated the inflammatory response, as evidenced by downregulating IL-6 and increasing IL-10 expressions in tissues. Furthermore, it improved liver functions and ameliorated the pathological alterations induced by trichinellosis. The best results were detected in combination treatments that indicated synergistic effects between EA and albendazole. In conclusion, EA can be used as an anti-inflammatory and antioxidant with a promising anti-parasitic impact against trichinellosis.

Spontaneous abortion (SA) is considered one of the most prevalent adverse outcomes of pregnancy. SA may occur due to genetic susceptibility and various maternal factors such as nutritional status. The aim of this study was to assess how dietary carotenoids and the FTO gene are related to SA. This case–control study included 192 women with a history of SA as the case group and 347 healthy women without history of SA as the control group. To evaluate carotenoid intake, a valid 168-item food frequency questionnaire (FFQ) was used. The FTO gene was genotyped for the presence of the rs9939609 polymorphism using the tetra-primer amplification refractory mutation system-polymerase chain (ARMS-PCR). The results indicated a significant negative association between dietary intake of β-cryptoxanthin and SA in carriers of the TT genotype of the FTO rs9939609 polymorphism after adjustment for age, BMI, physical activity, smoking, alcohol drinking, and calorie intake (β = −0.28, P = 0.02). No association was found between SA with dietary intake of beta-carotene, alpha-carotene, lutein, and lycopene among carriers of different FTO genotypes. The FTO genotype may have an effect on the association between SA and carotenoid intake. Dietary intake of β-cryptoxanthin may act as a protective factor against SA only in carriers of the TT genotype of the FTO rs9939609 polymorphism.

Oxidative stress may be involved in the progression of hypothyroidism in patients with Hashimoto thyroiditis (HT). Vitamin C is a well-known powerful antioxidant. To our knowledge, whether vitamin C intake relates to hypothyroidism in patients with HT remains unclear. In this cross-sectional study based on the National Health and Nutrition Examination Survey, 2007–2012, we aimed to explore the relationship between total vitamin C intake and hypothyroidism in patients with HT, using multivariate logistic regression models and restricted cubic spline analyses. Our results showed a significant negative linear association between total vitamin C intake (log10-transformed data) and hypothyroidism in HT. Compared with those with the lowest quartile of total vitamin C intake (log10-transformed), participants with the highest quartile were at lower odds of having hypothyroidism (adjusted OR 0·40, 95 % CI: 0·18, 0·88, Ptrend = 0·027). This association was consistent in subgroups stratified by sex (Pfor interaction = 0·084) and age (≥ 60 years and < 60 years, Pfor interaction = 0·330). This study revealed that total vitamin C intake was inversely associated with hypothyroidism among individuals with HT, indicating that higher vitamin C intakes (4·57–1258·9 mg/d) may be associated with a lower likelihood of hypothyroidism among HT participants.

A positive association has been demonstrated between consumption of sucrose-sweetened beverages and the prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD). Since the administration of 30 % sucrose in the drinking water (sucrose-rich diet (SRD)) to rats has proven to be a good model of systemic insulin resistance, the aim of our study was to analyse the effect of caloric restriction applied on SRD-treated rats by switching back to a standard diet, on liver morphology, function and metabolism. Consumption of an SRD causes a metabolic shift towards gluconeogenesis and fatty acid synthesis leading to an increase in TAG levels in plasma and in the liver that were associated with a decrease in insulin sensitivity. Moreover, our results show that animals fed an SRD develop steatohepatitis characterised by the generation of oxidative stress, endoplasmic reticulum (ER) stress, inflammation and apoptosis. Although no histological changes were observed after a 2-week caloric restriction, key pathways associated with the progression of MASLD as inflammation, ER stress and apoptosis were slowed down. Notably, this 2-week intervention also increased liver insulin sensitivity (evaluated by AKT activity in this tissue) and drove the lipid metabolic profile towards oxidation, thus lowering circulating TAG levels. In summary, the present study uncovers underlying mechanisms affected, and their metabolic consequences, during the first stages of the phenotypic reversal of steatohepatitis by switching back to a standard diet after receiving sucrose-sweetened water for several weeks.

This study evaluated the effect of green tea extract and metformin and its interaction on markers of oxidative stress and inflammation in overweight women with insulin resistance. After screening, 120 women were randomly allocated in 4 groups: Placebo (PC): 1g of microcrystalline cellulose/day; Green tea (GT): 1 g (558 mg polyphenols) of standardized dry extract of green tea/day and 1 g of placebo/day; Metformin (MF): 1 g of metformin/day and 1 g of placebo/day; Green Tea and Metformin (GTMF): 1 g (558 mg polyphenols) and 1 g of metformin/day. All groups were followed-up for 12 weeks with assessment of oxidative damage to lipids and proteins, specific activity of antioxidant enzymes and inflammatory cytokine serum levels. The association of green tea with metformin significantly reduced IL-6 (GTMF: –29.7((–62.6)–20.2))(p = 0.004). Green tea and metformin isolated reduced TNF-α (GT: –12.1((–18.0)–(–3.5)); MF: –24.5((–38.60)–(–4.4)) compared to placebo (PB: 13.8 (1.2–29.2))(P < 0.001). Also, isolated metformin reduced TGF-β (MF: –25.1((–64.4)–0.04)) in comparison to placebo (PB: 6.3((–1.0)–16.3))(p = 0.038). However, when combined, their effects were nullified either for TNF-α (GTMF: 6.0((–5.7)–23.9) and for TGF-β (GTMF: –1.8((–32.1)–8.5). This study showed that there is a drug-nutrient interaction between green tea and metformin that is dependent on the cytokine analyzed.