Search Results (877)

This study investigated the effects of vitamin E supplementation on growth performance, antioxidant capacity, and hepatic lipid metabolism in one-year-old juvenile Chinese sturgeon (Acipenser sinensis). A total of 270 fish (initial weight 1.37 ± 0.04 kg) were allocated into 9 fiberglass tanks and fed isonitrogenous and isolipidic diets with graded concentrations of vitamin E (DL-α-tocopherol acetate) including, 0, 1000, and 2000 mg/kg, respectively, for 2 months. Results showed that 1000 mg/kg vitamin E significantly improved growth performance and decreased hepatosomatic index. Dietary vitamin E supplementation significantly reduced the hepatic crude protein and crude lipid levels, withnot significantly affecting moisture and crude ash. Dietary vitamin E led to significant increases in plasma high-density lipoprotein cholesterol and vitamin E levels, while decreasing plasma low-density lipoprotein cholesterol. Additionally, it raised liver vitamin E content and reduced hepatic triglycerides, total cholesterol, crude protein, and crude lipid levels. Vitamin E also significantly downregulated mRNA levels of lipogenesis-related genes (ACC1, acetyl-CoA carboxylase 1; FASN, fatty acid synthase; and PPARγ, peroxisome proliferator activated receptor γ) and inhibited the enzyme activities of ACC1 and FASN, while upregulating lipolysis-related genes (HSL, hormone-sensitive lipase; CPT1, carnitine palmitoyltransferase 1α, and PPARα, peroxisome proliferator activated receptor α) and enhancing the activities of HSL and CPT1α. Furthermore, vitamin E supplementation significantly improved plasma reduced glutathione and superoxide dismutase activities, lowered plasma reactive oxygen species, malondialdehyde levels, and hepatic malondialdehyde contents, and upregulated mRNA levels of hepatic Nrf2 (nuclear factor-erythroid 2 related factor 2), Keap1 (Kelch-like epichlorohydrin associating protein 1), and CuZnSOD (copper/zinc superoxide dismutase). In conclusion, dietary 1000 mg/kg vitamin E supplementation could improve growth performance, enhance antioxidant capacity, and reduce liver fat deposition, indicating its potential as a beneficial dietary additive for promoting health and lipid regulation in juvenile Chinese sturgeon. Full article

The global burden of heart failure (HF) continues to escalate, with a lifetime risk approaching one in four adults in the United States. Concurrently, advances in cancer therapeutics have created a burgeoning population of long-term survivors, who now face the significant morbidity and mortality of chemotherapy-induced cardiovascular disease (CVD). This review addresses the critical overlap of these two pathologies, which share fundamental drivers such as oxidative stress, inflammation, and metabolic dysregulation. Epigallocatechin gallate (EGCG), the most abundant and biologically active polyphenol in green tea, has demonstrated pleiotropic bioactivity in preclinical models, encompassing potent antioxidant, anti-inflammatory, and anti-apoptotic properties. The central aim of this review is to provide a critical and comprehensive synthesis of the evidence supporting EGCG’s dual protective role. This review dissects its molecular mechanisms in modulating key pathways in HF and cardio-oncology, evaluates its translational potential, and importantly, delineates the significant gaps that must be addressed for its clinical application. This analysis uniquely positions EGCG not merely as a nutraceutical, but as a multi-target molecular therapeutic capable of simultaneously addressing the convergent pathological cascades of heart failure and cancer-related cardiotoxicity. The synthesis of preclinical evidence with a critical analysis of its translational barriers offers a novel perspective and a strategic roadmap for future research. Full article

Marine-derived proteins are important sources in the preparation of umami peptides due to their delicious and unique taste. The research endeavored to elucidate the established umami peptide library derived from Skipjack tuna protein through a combined approach of computational and experimental proteolysis. A total of five potential shared umami peptides (GVGGHGAGG, GVTGVG, GGVAGCQGK, MANR, and SPAAK) were identified through database and molecular docking, which revealed that hydrogen bonds and electrostatic forces critically influence the interaction between peptides and T1R1/T1R3. The specific amino acids within the T1R1/T1R3 corresponding to glutamic acid, serine, arginine, aspartic acid, and histidine significantly influenced the affinity for umami peptides. It was verified through sensory and electronic tongue analysis that all these peptides exhibit umami performance and flavor-enhancing effects. Furthermore, bioinformatic predictions and computer simulations exploring the biological activity of umami peptides revealed that GVGGHGAGG, GVTGVG, and GGVAGCQGK, combined with Keap1, presented potential antioxidant activity. These observations offered new insights for identifying bioactive umami peptides from aquatic products and a theoretical foundation for developing novel seasonings. Full article

Cervical cancer ranks as a primary contributor to cancer-related deaths in women globally and is the fourth most prevalent malignant neoplasm. Cepharanthine, a naturally occurring biscoclaurine alkaloid extracted from Stephania cepharantha, has demonstrated anticancer and antimetastatic efficacy across multiple cancer types. However, its mechanism of action in cervical cancer remains unexplored. Our results demonstrated that cepharanthine effectively suppressed the proliferation and motility of the CaSki, HeLa, and C33A cell lines. Furthermore, cepharanthine triggered apoptosis through Bcl-2 suppression and increased cleaved-PARP-1, Bax, and cleaved-caspase-3 expression and AMPK/p53 phosphorylation, while inducing G0/G1 phase arrest in CaSki cells and sub-G1 phase arrest in HeLa and C33A cells. Additionally, cepharanthine reduced the mitochondrial membrane potential (∆ψm), compromised mitochondrial functionality, and increased reactive oxygen species (ROS) accumulation, promoting oxidative stress via the modulation of the Nrf2/Keap1 pathway in CaSki, HeLa, and C33A cells, which exhibit an anti-cervical cancer effect. Similarly, cepharanthine markedly reduced tumor progression in C33A BALB/c nude mice, which aligns with the in vitro observations. Collectively, these findings indicate that cepharanthine has potential therapeutic applications in the treatment of cervical cancer and warrants future clinical investigation. Full article

Redox dysregulation, ferroptosis evasion, and immune suppression are major barriers in cancer therapy. SH003, a multi-herbal formulation standardized under GMP conditions and evaluated in early-phase clinical studies (NCT03081819; KCT0004770), demonstrated a favorable safety profile supporting its translational potential. Preclinical studies reveal that SH003 disrupts mitochondrial homeostasis, triggers endoplasmic reticulum stress apoptosis, and sensitizes resistant tumors to ferroptosis via suppression of the SLC7A11–GPX4 axis and NRF2 destabilization. In parallel, SH003 remodels tumor immunity by attenuating STAT3-driven PD-L1 signaling, promoting macrophage repolarization, and enhancing cytotoxic lymphocyte activity. Exosome-associated microRNAs further suggest SH003’s role in redox–immune communication, although functional validation is pending. Collectively, SH003 represents a clinically tested phytomedicine that integrates ferroptosis induction with immune modulation, offering a biomarker-informed approach to precision oncology. Full article

In this study, we constructed an extraction process for bovine lung peptide-1 (BLP-1) derived from bovine lung tissue utilizing single-factor optimization combined with response surface methodology. We systematically analyzed its antioxidant activity, biological safety, and therapeutic mechanisms against alcoholic liver disease (ALD). In vitro experiments demonstrated that BLP-1 exhibits excellent scavenging activity against various free radicals, while exhibiting no significant cytotoxicity or hemolytic activity. In a model of H₂O₂-induced oxidative damage in HepG2 cells, BLP-1 significantly alleviated oxidative stress injury by upregulating the activities of intracellular antioxidant enzymes. Animal experiments further confirmed that BLP-1 significantly reduced serum levels of transaminase, inhibited the release of inflammatory factors, enhanced antioxidant enzyme activity, and ameliorated lipid peroxidation and pathological injury in ALD mice. By combining liquid chromatography-tandem mass spectrometry (LC-MS/MS) with bioinformatics, we screened 12 novel antioxidant peptides. Among these, the binding energies of GP9, FG6, and WG6 to Keap1 were −10.2, −9.7, and −8.7 kcal/mol, respectively, indicating their potential to modulate the antioxidant defense system through competitive inhibition of Keap1-Nrf2 interactions. This study provides a novel approach for the high-value utilization of bovine lung and the treatment of ALD, as well as a new source for the extraction of natural antioxidant peptides. Full article

Various clinical studies aimed at modifying the progression of idiopathic Parkinson’s disease have been unsuccessful. Similarly, several nutritional trials using bioactive compounds have shown positive effects for patients but have also failed to slow or reduce the disease’s progression. This repeated failure is likely because these studies ignore the extremely slow neurodegenerative process, which unfolds over many years. The molecular mechanism behind the loss of neuromelanin-containing dopaminergic neurons in the nigrostriatal system in idiopathic Parkinson’s disease remains unclear. This is a conceptual/theoretical review based mainly on mechanistic and preclinical evidence, with no direct clinical data. However, research suggests that aminochrome, an endogenous neurotoxin, may trigger the degeneration of these neurons through a single-neuron degeneration model. In this model, aminochrome selectively destroys individual neurons without spreading to neighboring cells. Aminochrome is produced during neuromelanin synthesis, a process that is normally harmless because protective enzymes like DT-diaphorase and glutathione transferase M2-2 neutralize aminochrome’s neurotoxic effects. Increasing the levels of these enzymes could offer neuroprotection. The KEAP1/NRF2 signaling pathway is critical for regulating antioxidant enzymes, such as DT-diaphorase and glutathione transferase M2-2. Importantly, specific bioactive compounds from food can activate this pathway, increasing the production of these protective enzymes. For instance, the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), along with astaxanthin—a compound present in cold-water fish like salmon—have been demonstrated to enhance enzyme expression. This connection leads to a compelling question: Could dietary interventions help prevent idiopathic Parkinson’s disease? Answering this will require further research. Full article

Age-related macular degeneration (AMD) is a retinal degenerative disease caused by oxidative stress. Thus, we aimed to reduce oxidative stress through the use of placenta-derived mesenchymal stem cells (PD-MSCs). To induce oxidative stress in ARPE-19 cells, we treated them with 200 µM hydrogen peroxide (H₂O₂) for 2 h and then cocultured them with PD-MSCs. The dissociation of the KEAP1/Nrf2 complex, along with the expression of phosphoinositide 3-kinase (PI3K) and protein kinase B (AKT), increased in the coculture group compared with the H₂O₂ treatment group (* p < 0.05). The expression levels of antioxidant genes increased in the cocultured group compared with those in the H₂O₂ treatment group (* p < 0.05), whereas the ROS levels decreased in the cocultured group (* p < 0.05). Additionally, both the expression of mitochondrial dynamics markers and the mitochondrial membrane potential increased when the cells were cocultured with PD-MSCs (* p < 0.05). PD-MSC cocultivation decreased the expression levels of lipoproteins (* p < 0.05). Finally, we confirmed that PD-MSCs promoted the expression of RPE-specific genes in H₂O₂-injured ARPE-19 cells (* p < 0.05). These findings suggest a new aspect of stem cell treatment for AMD induced by oxidative stress. Full article

Background: Chronic stress is implicated in the pathogenesis of gastrointestinal disorders, with reactive oxygen species (ROS) contributing significantly. Chlorogenic acid (CGA), a polyphenolic compound, exhibits antioxidant properties. This study investigated whether CGA mitigates ROS-mediated oxidative stress and apoptosis in chronic stress-induced ileal injury. Methods: Rats were subjected to restraint stress for 21 days, with/without CGA (100 mg/kg, gavage). CGA’s mechanism was elucidated by assessing ileal flora, oxidative stress markers, apoptosis, structural changes, and the Nrf2 pathway. Results: CGA restored ileal structure, attenuated ROS and MDA levels, elevated GSH and SOD levels, and reduced apoptosis-associated proteins. CGA stabilized conformation bound to Keap1, deregulating Keap1’s negative regulation of Nrf2, thereby increasing Nrf2 and downstream protein expression (HO-1 and NQO1). Gut microbiota imbalance was corrected, with increased Lactobacillus abundance post-CGA intervention. Conclusions: CGA alleviates chronic stress-induced ileal oxidative stress and apoptosis, which relates closely to Nrf2 pathway activation and modulation of intestinal microflora. Full article

Hydroxytyrosol (HXT), a phenolic compound from olive, shows great potential as a neuroprotective agent and a translational target for claim-ready nutrition and food products. Human studies increasingly report benefits for vascular function, inflammatory tone, and early cognitive/psychomotor outcomes, consistent with engagement of redox and signalling pathways (Keap1–Nrf2–ARE, PI3K/Akt–ERK, and AMPK–SIRT1–PGC-1α). HXT is rapidly absorbed and likely reaches the brain, acting on endothelial and microglial targets. On the neurovascular axis, it reduces oxidative stress, preserves nitric-oxide bioavailability, lower inflammatory markers, and favourable intrinsic connectivity. For product development, bitterness from oleuropein-rich inputs can be mitigated by hydrolysis, followed by structure-guided delivery to balance sensory quality with exposure. Viable formats include cyclodextrin inclusion, microencapsulation, and (micro)emulsions in lipid matrices, plus stability engineering for aqueous systems (acidification, chelation, low-oxygen handling, or barrier packaging). Matrix effects are consequential; some proteins and fibers may decrease HXT bioaccessibility, whereas lipid phases and microstructured carriers often enhance it. Clinically, recommended doses are ~7–15 mg/day chronically and ~30–60 mg acutely. As conclusions of this review, future work should prioritize harmonized pharmacokinetics–pharmacodynamics readouts, cognition anchored to a compact neurovascular/blood–brain barrier biomarker core, and head-to-head comparisons of manufacturable delivery formats. Full article

An overproduction of reactive oxygen species (ROS) creates oxidative stress that disrupts neuronal activity and contributes to the pathogenesis of neurodegenerative diseases. Arecoline, the predominant alkaloid component of Areca catechu L., is known for multiple biological activities, yet its involvement in neuronal oxidative injury has not been fully clarified. This study investigated arecoline’s effect on hydrogen peroxide (H₂O₂)-induced toxicity in SH-SY5Y human neuroblastoma cells (SH-SY5Y). Arecoline pretreatment significantly improved cell viability and preserved plasma membrane integrity, accompanied by reduced lipid peroxidation and restoration of cellular antioxidant enzyme activities. Moreover, arecoline maintained mitochondrial membrane potential and suppressed apoptotic progression. At the molecular level, Arecoline stimulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) protein expression, concurrently diminishing Kelch-like ECH-associated protein 1 (Keap1) levels. In parallel, it altered the apoptosis profile by increasing B-cell lymphoma 2 (Bcl2) levels and decreasing Bcl-2-associated X protein (Bax) and total cysteine aspartate protease-3 (Caspase-3) protein expression. Collectively, the findings suggest that arecoline safeguards neurons against oxidative stress by simultaneously activating antioxidant defenses and restraining apoptosis. This study adds novel molecular evidence supporting the potential neuroprotective relevance of arecoline in oxidative stress-related neuropathology. 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

Corticosterone (CORT), a key stress hormone, is vital for energy balance, but prolonged exposure causes hyperglycemia, obesity, and hepatotoxicity. Gallic acid (GA), a natural polyphenol with antioxidant and anti-inflammatory properties, was evaluated for its hepatoprotective effects in Wistar rats. This study aimed to assess how GA protects against CORT-induced liver toxicity in Wistar rats and to explore its molecular interactions through in silico docking studies. Animals received CORT (15 and 30 mg kg⁻¹ body weight) orally for 21 days, with GA pretreatment in selected groups. Hepatic status was assessed via biochemical assays, molecular markers, histopathology, and in silico docking. CORT significantly increased body weight (15%), blood glucose (1.5-fold), malondialdehyde (MDA; 28%), and protein carbonyls (34%,) with a statistical significance, p < 0.05 and <0.01, while glutathione (41.4% to 52.1%) and antioxidant enzymes were significantly reduced (statistical p-value significance at levels of <0.05, <0.01, and <0.001). GA pretreatment restored glucose MDA, and GSH toward control (p < 0.01), and protected histological injury. Docking studies showed strong GA binding to Keap1 (−6.9 kcal/mol), IKKβ (−6.0 kcal/mol), and COX-1 (−6.2 kcal/mol), supporting its antioxidant and anti-inflammatory action. GA confers significant protection against CORT-induced hepatotoxicity, validated by both in vivo and in silico analyses. Full article

This study investigated the influence of two distinct aquaculture systems, namely, the wheat-crab model (WCM) and pond culture (PC) model, on the growth, physiological well-being, and gut microbial structure of Chinese mitten crabs (Eriocheir sinensis). A total of 120 adult crabs were randomly selected from the two systems: 60 crabs from the WCM, including 30 females and 30 males, and 60 crabs from the PC model, also including 30 females and 30 males. The gonadosomatic index of female crabs in the WCM was notably higher than that of the other groups, while the hepatopancreatic index was significantly lower. Significant variations were not observed in final weight, fullness, or muscle yield between the WCM and PC groups. Biochemical evaluations indicated no substantial differences in antioxidant capabilities between the two systems; however, female crabs demonstrated increased critical antioxidant enzyme activity, such as for catalase and superoxide dismutase, and significantly elevated cholesterol levels. Additionally, the expression of the genes IL, ProPO, and Keap1 was significantly higher in the WCM group than the PC group, whereas the expression of ALF2, Myd88, and CncC did not significantly differ between the two cultivation methods. Non-targeted metabolomics analysis revealed notable distinctions in metabolite profiles between the two systems. Moreover, the WCM facilitated an increase in beneficial Firmicutes bacteria while reducing potentially harmful microorganisms, suggesting improved immune function in crabs raised under the WCM. In summary, female crabs reared in the WCM matured earlier and exhibited slightly better health conditions compared to those grown in the PC model. Full article

Introduction: Bisphenol A (BPA) is a synthetic compound widely used in plastics and epoxy resins, and human exposure is virtually unavoidable. Numerous studies indicate that even doses below current regulatory limits may elicit neurotoxic effects, impairing learning, memory, and synaptic plasticity. Methodology: This mini-review. Searches were conducted in PubMed, the Virtual Health Library (VHL/BVS), and ScienceDirect, using MeSH descriptors related to “Bisphenol A,” “Neurotoxicity Syndromes,” “Central Nervous System,” and “Prefrontal Cortex,” combined with Boolean operators. We included studies published between 2007 and 2025, available in English, Portuguese, or Spanish, and focused on the neurotoxic effects of BPA. After screening and application of the eligibility criteria, twelve articles were selected. Results: The analyzed studies show that BPA exposure, even at low concentrations, compromises neuronal survival, dendritic density, and synaptic plasticity. In animal models, cognitive deficits were observed in memory and learning tasks, associated with increased oxidative stress and alterations in molecular pathways such as AMPK, HO-1, and nNOS/Keap1/Nrf2. In cell cultures, BPA induced apoptosis, autophagy dysfunction, cytoskeletal reorganization, and loss of synaptic proteins. The effects were dose-dependent and, in some cases, sex-dependent. Conclusions: BPA exhibits significant neurotoxic potential, affecting both the development and function of the central nervous system. These findings underscore the need to revise current safety limits and reinforce the importance of public policies regulating BPA use, as well as encouraging the search for safer alternatives. Full article