Search Results (2,561)

Sepsis-induced acute lung injury (SALI) is characterized by dysregulated inflammation with limited therapeutic options. Although Anemoside B4 (AB4) exhibits anti-inflammatory properties, its clinical application is hindered by poor bioavailability. To address this limitation, we developed magnetically guided gelatin microrobots (MG-AB4) for targeted AB4 delivery. The MG-AB4 system consists of a Fe₃O₄-loaded gelatin shell for enabling precise magnetic navigation (velocity: 110 μm/s), an AB4 core for rapid drug release which is advantageous for acute inflammatory responses, and surface modifications to enhance cellular uptake. Compared with free AB4, MG-AB4 significantly suppressed key inflammatory cytokines (Interleukin-6 (IL-6), Interleukin-1 beta (IL-1β), Tumor necrosis factor-alpha (TNF-α); p < 0.01), inhibited NF-κB activation (p < 0.01), and improved cell viability in an inflammatory model (p < 0.05). This study demonstrates that magnetically guided AB4 delivery using rapidly releasing microrobots is a promising strategy for SALI treatment, wherein the synergy of targeted delivery and potent anti-inflammatory action may effectively mitigate disease progression. Full article

The growing global aging population is contributing to an increasing burden of benign prostatic hyperplasia (BPH), highlighting the need for novel, highly effective and low-toxicity therapies. In light of its well-documented anti-inflammatory and anti-tumor properties, we investigated the potential of the natural product Pulsatilla saponin D (PSD) in treating BPH. For the first time, we demonstrate that PSD significantly inhibits the proliferation of and induces apoptosis in the immortalized human normal prostatic stromal cell line, human prostate fibroblasts, and the human benign prostatic hyperplasia epithelial cell line. Mechanistic studies involving transcriptome analysis and RT-qPCR validation revealed that PSD likely exerts its effects by downregulating the expression of the androgen receptor and by modulating multiple signaling pathways synergistically, including the Phosphatidylinositol 3-kinase/Protein Kinase B, Tumor Necrosis Factor, Hypoxia-Inducible Factor-1 and Interleukin-17 pathways. Full article

Eleutheroside E (EE), a natural compound, shows promise in mitigating cellular senescence—a key factor in skin aging—though its mechanisms remain incompletely understood. This study integrated network pharmacology, molecular docking, and cellular experiments to explore the protective effects and mechanistic basis of EE against D-galactose (D-gal)-induced senescence in human skin fibroblasts (HSFs). Network pharmacology analyses suggested EE’s involvement in inflammation-related pathways, especially phosphatidylinositol 3-kinase and protein kinase B (PI3K-AKT) and hypoxia-inducible factor 1 (HIF-1) signaling, which were corroborated by molecular docking revealing strong binding affinities between EE and key targets such as hypoxia-inducible factor 1-alpha (HIF1A), AKT serine/threonine kinase 1 (AKT1), phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma (PI3Kγ), and interleukin-6 (IL-6). Cellular assays showed that EE markedly lowered oxidative stress markers, including reactive oxygen species (ROS) and malondialdehyde (MDA), reduced senescence-associated beta-galactosidase (SA-β-gal) activity, and boosted antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT). Additionally, EE dose-dependently inhibited apoptosis and downregulated PI3K/AKT phosphorylation as well as the B-cell lymphoma 2-associated X protein/B-cell lymphoma-2 (Bax/Bcl-2) ratio. These findings suggest that EE alleviates cellular senescence in HSFs mainly via the PI3K/AKT pathway by attenuating oxidative stress and apoptosis, highlighting its potential as a therapeutic agent for anti-aging strategies. Full article

The study evaluated the influence of dietary supplementation with nano-encapsulated cumin oil, B. subtilis, or a combination of both to mitigate the impacts of heat stress on the performance and health of growing rabbits. In the feeding trial, a total of eighty-four growing New Zealand White (35 days, 781.3 ± 1.8 g average body weight) were randomly distributed in a completely randomized design into four groups; each had 21 rabbits arranged in 7 replicates (3 rabbits each). The experiment lasted 42 days (35 days to 77 days). Growing rabbits received a basal diet (first group, CON) without additives, while the other groups were supplemented with nano-encapsulated cumin oil (NECO, 200 mg/kg), B. subtilis (BS, 500 mg/kg), or both (BSNO, 500 mg BS plus 200 mg/kg NECO). Adding BSNO significantly enhanced body weight gain, carcass weight, and feed conversion ratio and reduced mortality rate (p < 0.05). Additionally, the BSNO enhanced digestive system performance by increasing the secretion of trypsin enzymes, as well as nutrient digestibility, especially for protein and fiber (p < 0.05). Supplementing BSNO enhanced oxidative stability and immunity via higher levels of superoxide dismutase (SOD), IgA, IgG, triiodothyronine (T3), thyroxine (T4) and lower malondialdehyde (MDA) levels (p < 0.05), indicating a better ability to adapt to stress. During the examination of gut health, pathogenic bacteria counts decreased, as well as down-regulation of interleukin-6 (IL-6) gene expression and up-regulation of cationic amino acid transporter-1 (CAT-1), interleukin-10 (IL-10), and mucin-2 (MUC-2) gene expression (p < 0.05), supporting gut integrity. This study highlights the potential of mixing nano-encapsulated cumin oil and B. subtilis in growing rabbits’ diets as an effective strategy to counteract the negative effects of heat stress caused by high ambient temperatures. Full article

High Mobility Group Box 1 (HMGB1) is a central pro-inflammatory mediator released from damaged or stressed cells, where it activates receptors such as the Receptor for Advanced Glycation Endproducts (RAGE). Dendritic polyglycerol sulfate (dPGS), a hyperbranched polyanionic polymer, is known for its anti-inflammatory activity. In this study, we examined how dPGS modulates HMGB1-driven signaling in RAW 264.7 macrophages and human microglia. Recombinant human HMGB1 expressed in Escherichia coli (E. coli) was purified by nickel-nitrilotriacetic acid (Ni-NTA) and heparin chromatography. Proximity ligation assays (PLA) revealed that dPGS significantly disrupted HMGB1/RAGE interactions, particularly under lipopolysaccharide (LPS) stimulation, thereby reducing inflammatory signaling complex formation. This correlated with reduced activation of the nuclear factor kappa B (NF-κB) pathway, demonstrated by decreased nuclear translocation and transcriptional activity. Reverse transcription polymerase chain reaction (RT-PCR) and quantitative real-time PCR (RT-qPCR) showed that dPGS suppressed HMGB1- and LPS-induced transcription of tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). Enzyme-linked immunosorbent assay (ELISA) and Griess assays confirmed reduced TNF-α secretion and nitric oxide production. Electron paramagnetic resonance (EPR) spectroscopy further showed that dPGS altered HMGB1/soluble RAGE (sRAGE) complex dynamics, providing mechanistic insight into its receptor-disruptive action. Full article

Background: Lupus nephritis (LN), a severe complication of systemic lupus erythematosus (SLE), necessitates effective therapeutic strategies. Polysaccharides derived from Irpex lacteus have demonstrated beneficial biological activities in MRL/lpr mice; however, their precise mechanisms of intervention in LN require further elucidation. Methods: MRL/lpr mice were administered low-dose and high-dose Irpex lacteus polysaccharide (PCP) continuously for 8 weeks. The therapeutic efficacy of PCP was systematically assessed by measuring autoantibody levels, inflammatory cytokine expression, and renal function markers. The underlying pharmacological mechanisms were investigated through integrated transcriptomics and metabolomics analyses. Results: PCP treatment significantly improved renal function in MRL/lpr mice, normalizing serum levels of anti-nuclear antibodies (ANA), anti-double-stranded DNA antibodies (anti-dsDNA), anti-Sm antibody (Sm), creatinine (Cr), blood urea nitrogen (BUN), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and proteinuria. Integrated transcriptomic and metabolomic analyses revealed that the therapeutic action of PCP involves modulation of the PI3K/AKT/NF-κB pathway. This inhibition was further confirmed by Western blot analysis. Conclusions: PCP exerts renal protective effects in MRL/lpr mice by mitigating inflammation, modulating immune responses, and preserving renal function. The combined application of transcriptomics, metabolomics, and Western blotting elucidates that this protection is mediated through inhibition of the PI3K/AKT/NF-κB signaling pathway. Full article

Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that significantly increases the risk of stroke, with prediabetes serving as an intermediate stage marked by similar pathophysiological mechanisms such as inflammation and vascular dysfunction. This study investigated the relationship between prediabetes and stroke-related biomarkers in individuals aged 25–45 years in Durban, South Africa. After obtaining ethical approval, a retrospective analysis was performed on blood samples from 100 participants recruited from King Edward Hospital and Inkosi Albert Luthuli Central Hospital. Participants were classified as non-prediabetic (n = 30), prediabetic (n = 35), or type 2 diabetic (n = 35) according to ADA criteria. Plasma concentrations of C-reactive protein (CRP), interleukin-6 (IL-6), fibrinogen, D-dimer, calcium binding protein (S100B), glial fibrillary acidic protein (GFAP), and neuron-specific enolase (NSE) were measured using enzyme-linked immunosorbent assay (ELISA). It is important to note that none of the participants had confirmed stroke events; these biomarkers were assessed as surrogate indicators of stroke risk. Statistical analyses included one-way ANOVA with Tukey–Kramer tests and Pearson’s correlations. Biomarker concentrations were significantly elevated in prediabetic individuals compared to non-prediabetic controls, with levels further increasing in T2DM. Strong positive correlations were observed between S100B and both HbA1c (r = 0.75, p < 0.0001) and fasting glucose (r = 0.75, p < 0.0001). These findings suggest that inflammatory, coagulation, and neurovascular biomarkers, particularly S100B, may indicate early stroke risk in prediabetes. Further investigation into these biomarkers could improve early detection strategies and stroke prevention efforts in at-risk populations. Full article

This research explored the effects of supplementing taurine in a low-fishmeal diet on the growth, hepatic antioxidant capacity, muscle quality, intestinal health, and alleviation of inflammatory response of golden pompano (Trachinotus ovatus). Over an eight-week period, 300 juvenile fish (initial weight 9.4 ± 0.47 g) were randomly allocated into 12 net enclosures (1.0 × 1.0 × 1.5 m), with each treatment group comprising three replicate cages containing 25 specimens. The results demonstrated that an optimal taurine inclusion level of 1.0–1.5% significantly promoted growth, as evidenced by the increased weight gain rate (WGR) and specific growth rate (SGR). It also protected hepatic health by reducing alanine aminotransferase (ALT) activity and enhancing antioxidant capacity. Activation of the hepatic Nrf2/Keap-1/HO-1 signaling pathway increased the level of antioxidant gene expression, including catalase (CAT) and superoxide dismutase (SOD). In addition, the appropriate supplementation of taurine significantly down-regulated muscle hardness-related genes (cathepsin B (CatB) and cathepsin L (CatL)) and promoted the growth and differentiation of myoblasts, thus improving muscle quality. The chymotrypsin of fish fed the A25T10 diet was significantly higher than those in other groups (p < 0.05). The amylase (AMY) of fish fed the A25T15 diet was significantly higher than those in other groups (p < 0.05). The Chao1, Shannon, and Simpson of fish fed the A25T15 diet were significantly higher than those in other groups (p < 0.05). Proteobacteria were the most abundant in group A25T10. The relative abundance of Photobacterium rose in the A25RT10 group. In this study, taurine supplementation can down-regulate the expression of intestinal pro-inflammatory factors (interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), interleukin-8 (IL-8)) and up-regulate the expression of anti-inflammatory factor interleukin-10 (IL-10), enhance intestinal immunity, and improve intestinal digestion and absorption. Therefore, the addition of 1–1.5% taurine to low-fishmeal feeds can improve the growth performance of golden pompano. Full article

Background: Chronic lymphocytic leukemia (CLL) is characterized by malignant B lymphocyte accumulation and progressive immune dysfunction. The immune checkpoint molecule TIM-3 and its ligand galectin-9 (Gal-9) contribute to T cell exhaustion, impairing anti-tumour immunity. Interleukin-27 (IL-27) has pleiotropic immunomodulatory properties, but its impact on TIM-3 and Gal-9 expression in CLL remains unclear. Methods: Peripheral blood mononuclear cells (PBMCs) from 20 treatment-naive CLL patients were cultured with or without IL-27 (100 ng/mL) for 72 h. Flow cytometry assessed TIM-3 and Gal-9 expression on CD4⁺, CD8⁺, and CD19⁺ cells. Results: IL-27 stimulation significantly increased TIM-3 expression on CD8⁺ T cells (2.18 ± 0.32% vs. 3.09 ± 0.49%, p = 0.009), a hallmark of T cell exhaustion. IL-27 also modestly increased intracellular Gal-9 levels in total lymphocytes (93.91 ± 1.17% vs. 96.55 ± 0.67%, p = 0.005). Additionally, IL-27 reduced CD4⁺ T cell proportions (26.71 ± 4.19% vs. 22.01 ± 3.23%, p = 0.010). Although numerically modest, these changes may be biologically pertinent in the context of checkpoint-mediated CD8⁺ T-cell exhaustion. Conclusions: IL-27 may enhance immunosuppressive mechanisms in CLL by modulating immune checkpoint expression, potentially contributing to disease progression. These ex vivo findings in PBMCs from CLL patients indicate the IL-27-associated modulation of checkpoint expression under the conditions tested. In the absence of parallel healthy-donor controls, CLL specificity cannot be established in this study. Full article

Background/Objectives: Hepatotoxicity remains a major therapeutic challenge driven by oxidative stress and inflammation. This study investigated the hepatoprotective potential of green-synthesized silver nanoparticles derived from ethanolic garlic peel extract (GPE-Ag) against pyrogallol-induced liver injury. Methods: Adult rats were randomly assigned into four groups: a control group, a pyrogallol-treated group, a group receiving GPE-Ag nanoparticles (50 mg/kg, orally) for 28 days, and GPE-Ag + pyrogallol co-treated. Results: The garlic peel extract was analyzed by high-performance liquid chromatography (HPLC), revealing high levels of phenolic acids (66.83 µg/g) and flavonoids (59.81 µg/g), predominantly ellagic, gallic, and syringic acids, along with kaempferol, quercetin, and myricetin. The synthesized GPE-Ag nanoparticles were characterized using UV–Vis spectroscopy, transmission and scanning electron microscopy (TEM and SEM), zeta potential, dynamic light scattering (DLS), and energy-dispersive X-ray analysis (EDAX). GPE-Ag treatment markedly attenuated pyrogallol-induced hepatic injury by reducing serum liver enzyme levels, lipid peroxidation, and proinflammatory cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), and nuclear factor-kappa B (NF-κB), while enhancing the activities of antioxidant enzymes, catalase (CAT) and glutathione peroxidase (GPx), as well as the anti-inflammatory cytokine interleukin-10 (IL-10). Histological examination further confirmed the restoration of normal hepatic architecture. Conclusion: This study provides the first evidence that garlic peel–derived silver nanoparticles exert potent hepatoprotective effects through redox homeostasis restoration and modulation of the NF-κB signaling pathway. These findings highlight GPE-Ag as a promising, sustainable nanotherapeutic candidate for managing chemically induced liver injury. Full article

Hormonal alterations associated with polycystic ovary syndrome (PCOS) also impact bone metabolism, though it is unclear if this is bone-protective or not. Bone marker dysfunction has been reported in PCOS and appears to be associated with obesity. This study sought to determine whether a panel of bone marker proteins (BMPs) would be dysregulated in PCOS stratified by BMI as a potential biomarker for bone in PCOS. In this exploratory cross-sectional study, plasma was collected from 234 women (137 with PCOS and 97 controls) from a biobank cohort and compared to a nonobese, non-insulin resistant population (24 with PCOS and 24 controls). Slow Off-rate Modified Aptamer (SOMA)-scan plasma protein measurement was undertaken for the following BMPs: sclerostin; Dickkopf-related protein-1; glycogen synthase kinase-3 alpha/beta; periostin; tumor necrosis factor ligand superfamily member 11; fibroblast growth factor 23; sphingosine kinase 1; sphingosine kinase 2; cathepsins A, B, D, E, G, L2, S and Z; parathyroid hormone; osteocalcin; tumor necrosis factor ligand superfamily member 11 (sRANKL) and interleukin-1 beta. Four BMPs differed in the PCOS cohort (whole set without matching for body mass index (BMI) or insulin resistance (IR)): periostin (p = 0.05), cathepsin L (p = 0.05) and osteocalcin (p = 0.02) decreased in PCOS, whilst cathepsin D (p = 0.02) increased; however, linear regression showed that only cathepsins D and L and osteocalcin differed. None of the BMPs differed in the nonobese women with and without PCOS, nor in obese PCOS and controls stratified by BMI greater than 30 kg/m². In subgroup analysis, periostin (p = 0.001), sphingosine kinase 2 (p = 0.01) and cathepsin L (p = 0.001) were higher in obese versus nonobese PCOS (p = 0.01). Cathepsin Z (p = 0.02), sphingosine kinase 2 (p = 0.04) and lysosomal protective protein (p = 0.05) were lower in obese versus nonobese controls. Changes in BMPs indicative of impaired bone physiology were associated with BMI in both controls and PCOS, but did not differ between women with and without PCOS when BMI was matched. Hyperandrogenemia in PCOS did not affect BMP levels. Full article

Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by cartilage degradation, synovial inflammation, and subchondral bone remodeling, leading to chronic pain and reduced mobility. In early-stage OA, sustained oxidative stress and inflammation drive chondrocyte dysfunction and extracellular matrix (ECM) loss. Hyaluronic acid (HA), a key component of synovial fluid responsible for lubrication and viscoelasticity, is prone to enzymatic and oxidative degradation under inflammatory conditions, limiting its therapeutic effect. To address this, we developed an HA-based system incorporating the natural antioxidant and anti-inflammatory molecule carvacrol. The potential of this formulation was assessed in interleukin-1b-stimulated chondrocytes, which mimic the inflammatory environment of OA. The carvacrol-added HA combination upregulated antioxidant enzyme expression, attenuated pro-inflammatory signaling, and promoted ECM preservation by up regulating cartilage-specific markers and glycosaminoglycan production. In vivo efficacy was further evaluated in a rat model of monosodium iodoacetate-induced OA. HA-Carvacrol treatment alleviated pain-related behaviors and preserved cartilage structure, as confirmed by behavioral assessments and histological analyses. This dual-function formulation integrates the lubricating benefits of HA with the bioactivity of carvacrol, providing preclinical proof-of-concept evidence for its potential in early-stage OA. Full article

Thiotaurine (2-aminoethane thiosulfonate) is a naturally occurring sulfur-based compound featuring a thiosulfonate group, enabling it to act as a biologically relevant donor of hydrogen sulfide (H₂S) through thiol-dependent persulfidation. H₂S levels are known to be reduced in individuals with osteoarthritis, where it plays roles in modulating inflammation, oxidative stress, and pain. This study investigated the anti-inflammatory effects of Thiotaurine in human primary chondrocytes exposed to a pro-inflammatory cytokine. Cells were pre-treated with Thiotaurine prior to stimulation with TNF-α, and the expression levels of key interleukins were assessed at both the mRNA and protein levels. TNF-α stimulation led to upregulation of IL-6, IL-8, and IL-1β, which was significantly attenuated by Thiotaurine pre-treatment. Additionally, immunofluorescence analysis showed that Thiotaurine inhibited the phosphorylation and nuclear translocation of p65, indicating suppression of NF-κB pathway activation. Persulfide detection assays confirmed an increase in intracellular persulfide levels following Thiotaurine treatment. In summary, due to its anti-inflammatory activity and ability to release H₂S, Thiotaurine emerges as a promising and potentially safe therapeutic option for osteoarthritis and other inflammation-related conditions. Full article

Food-derived bioactive peptides are known to possess immunomodulatory properties, although their molecular mechanisms remain incompletely characterized. In this study, we investigated the immunoregulatory effects and underlying mechanisms of YPFPGPIH, a peptide derived from bovine β-casein, using the RAW264.7 macrophage model. Our results demonstrate that YPFPGPIH enhanced macrophage proliferation and phagocytosis in a dose-dependent manner and promoted chemotactic migration through the upregulation of monocyte chemoattractant proteins MCP-1 and MCP-3. Under lipopolysaccharide (LPS)-induced inflammatory conditions, YPFPGPIH significantly reduced the levels of pro-inflammatory mediators, including interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and nitric oxide (NO), while increasing the production of the anti-inflammatory cytokine interleukin-10 (IL-10), thereby reestablishing cytokine balance. Mechanistic studies revealed that YPFPGPIH inhibited LPS-induced activation of the NF-κB and MAPK pathways, as indicated by reduced nuclear translocation of p65 and decreased phosphorylation of ERK, JNK, and p38. Molecular docking analysis indicated strong binding affinities between YPFPGPIH and Toll-like receptors TLR2 and TLR4, suggesting the involvement of TLR-mediated signaling. Notably, YPFPGPIH downregulated inducible nitric oxide synthase (iNOS) expression and upregulated chemokine mRNA levels, reflecting its dual role in modulating inflammatory and migratory responses. These findings highlight YPFPGPIH as a multifunctional immunomodulatory peptide that fine-tunes macrophage activity through crosstalk between TLR, NF-κB, and MAPK signaling pathways. This study provides new insights for developing peptide-based therapeutics and functional foods aimed at managing inflammatory diseases. Full article

Mercury exposure has been linked to male infertility. Given that mercury chloride (HgCl₂) may promote an oxido-inflammatory milieu associated with pathophysiological derangements, it is hypothesised that Thymoquinone (TQ), an antioxidant and anti-inflammatory agent, may mitigate the gradual harmful effects of mercury exposure on rat testes, epididymis, and hypothalamus, as these organs are vital to reproductive function. To test this hypothesis, 40 rats (strain: Wistar; sex: male) were randomly assigned to five cohorts of eight rats each. After a 7-day acclimation, treatments were dispensed for 28 consecutive days accordingly: Cohort I: distilled water only, as control; Cohort II: HgCl₂ only (20 µg/mL); Cohort III: TQ only (2.5 mg/kg); Cohort IV: HgCl₂ + TQ (20 µg/mL + 2.5 mg/kg); and Cohort V: HgCl₂ + TQ (20 µg/mL + 5 mg/kg). Co-treatment with TQ preserved the body and organ weight of the HgCl₂ exposed animals. However, TQ did not reduce HgCl₂-induced dysfunction in sperm function and morphology. The serum follicle-stimulating hormone (FSH), luteinising hormone (LH), and testosterone were increased significantly (p < 0.05) by TQ co-treatment, while decreasing the prolactin level. TQ administration also increased (p < 0.05) testicular enzymes, including alkaline phosphatase (ALP), lactate dehydrogenase (LDH), acid phosphatase (ACP), and glucose-6-phosphate dehydrogenase (G6PD) activities, which HgCl₂ decreased. TQ administration increased (p < 0.05) HgCl₂-induced decreases in catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione (GSH), glutathione-s-transferase (GST), and total sulfhydryl group (TSH) levels in the testes, epididymis, and hypothalamus of experimental rats. Further, TQ reduced HgCl₂-mediated increases in RONS-reactive oxygen and nitrogen species; LPO–lipid peroxidation; PC–protein carbonyl formation; and XO–xanthine oxidase activity. Furthermore, levels of inflammatory biomarkers, including tumour necrosis factor alpha (TNF-α), nitric oxide (NO), interleukin-1 beta (IL-1β), and myeloperoxidase (MPO), were decreased (p < 0.05) in the co-treated groups, with a higher dose of TQ (5.0 mg/kg) showing a more pronounced protective effect. Additionally, TQ co-administration increased Bax and decreased Bcl-2 and p53 protein levels (p < 0.05), thereby protecting the rats’ testes, epididymis, and hypothalamus from HgCl₂-induced apoptosis. Molecular docking simulation analysis revealed TQ interaction dynamics with PPAR-α and PPAR-δ to suppress NF-kB-mediated pro-inflammatory sequela as well as activate Nrf-2-mediated antioxidant defence system. These predicted biological effects of TQ resonate with the findings from the in vivo studies. Therefore, supplementation with TQ may help reduce chemical-induced toxicities, including HgCl₂‘s reproductive toxicity. Full article