Antioxidants最新文献

Metabolic syndrome (MetS) represents a global health challenge mainly driven by chronic low-grade inflammation and persistent oxidative stress (OS). Current therapeutic and nutritional strategies often fail to resolve these interconnected core pathologies due to the multifactorial nature of MetS. Anthocyanins (ACNs), a class of potent dietary flavonoids, offer significant promise due to their established pleiotropic effects, including robust antioxidant activity through modulation of the Nrf2/ARE pathway, anti-inflammatory effects via NF-κB suppression, and overall support for glucose and lipid homeostasis. However, the therapeutic efficacy of ACNs is characterized by interindividual variability, which is intrinsically linked to their low systemic bioavailability. This heterogeneity in the response is due to the complex interplay between genetic polymorphisms affecting absorption, distribution, metabolism, and excretion (ADME), as well as the specific biotransformation capacity of the gut microbiome. This review proposes that achieving the full clinical potential of ACNs requires moving beyond conventional nutritional advice. We propose that precision nutrition, which integrates multi-omics data (e.g., genomics, metagenomics, and metabolomics), can determine the individual phenotype, predict functional metabolic response, and tailor safer and effective ACN-rich interventions. This integrated, multifactorial approach is essential for optimizing the antioxidant and metabolic benefits of ACNs for the prevention and management of MetS and its associated pathologies.

Obesity is a foremost risk factor for the development of cardiovascular disease, a hallmark of which is chronic vascular inflammation and overproduction of reactive oxygen species (ROS). NADPH oxidases (NOX) are central mediators of ROS overproduction in the obese vasculature, yet a complete understanding of the mechanism underlying their dysregulation in obesity remains poorly understood. Herein, we investigated the contribution of NOX1 in obesity-associated hypertension and evaluated the therapeutic potential of pharmacologically targeting NOX1 using the novel inhibitor GKT771. In obese db/db mice, NOX1 deletion ameliorated hypertension independent of metabolic improvements such as weight loss or improved glucose handling. Furthermore, NOX1 deletion improved renal sodium handling with no compensatory upregulation of other NOX isoforms. Importantly, treatment with the NOX1-specific inhibitor GKT771 rescued endothelial function in obese mice, restoring microvascular function to levels observed in lean controls. These data highlight the importance of NOX1 as a driver of endothelial dysfunction in obesity and suggest that NOX1 inhibition may offer a novel therapeutic strategy for obesity-associated endothelial dysfunction and its downstream cardiovascular complications.

Parkinson's disease is the second most common neurodegenerative disease in the world. Natural products can offer a possible option of neuroprotective agents for preventing neurodegenerative diseases. D-Pinitol is a cyclic polyol with anxiolytic and antidepressant effects in acute assays. This work aimed to evaluate the effects of D-Pinitol (10, 50, and 100 mg/kg p.o.) in a chronic reserpine-induced depression model (19 days), using the forced swimming and tail suspension tests in female Balb/c mice, and the neuroprotective effects in an MPTP-induced Parkinsonism model (30 days) in male C57bL/6 mice, using behavioral tests such as wire grip, rotarod, catalepsy, and others. D-Pinitol showed low antidepressant-like effects in the reserpine-induced chronic depression model, compared to amitriptyline (25 mg/kg p.o.). D-Pinitol protected MPTP-treated mice from motor impairment with similar effects to those shown by L-Dopa (25 mg/kg p.o.) as evaluated in different behavioral tests. The inhibition of oxidative stress markers, increase in dopamine levels, and avoidance of apoptosis in neuronal cells were the mechanisms by which D-Pinitol protects MPTP-treated mice from motor impairment.

Background: Arginase influences cardiac tolerance to ischemia-reperfusion by modulating nitric oxide (NO) signaling. In type 2 diabetes (T2D), elevated arginase activity may worsen ischemic injury through red blood cells (RBCs), but the specific roles of arginase isoforms are unclear.

Methods: C57BL/6 and db/db mice were pretreated with ARG1 or ARG2 antisense oligonucleotides (ASO) for six weeks. Conditional ARG1 knockout (ARG1^fl/fl/Tie2Cre^tg/-) and wild-type littermates were also studied. Mice underwent coronary artery ligation and reperfusion in vivo for infarct size assessment. In ex vivo experiments, buffer-perfused hearts were subjected to global ischemia-reperfusion with or without RBCs to evaluate recovery of left ventricular developed pressure (LVDP).

Results: ARG1 knockdown, but not ARG2, improved post-ischemic recovery of LVDP in isolated hearts. RBCs from ARG1 ASO-treated mice enhanced recovery in wild-type hearts, while ARG1 knockout reduced infarct size compared with controls. Cardioprotection was abolished by NO synthase inhibition. RBCs from male and female ARG1 knockout mice improved LVDP recovery compared with RBCs from wild-type mice. In T2D mice, impaired recovery was restored by ARG1 ASO or RBCs from ARG1 ASO-treated T2D mice.

Conclusions: Arginase 1, but not arginase 2, limits cardiac tolerance to ischemia-reperfusion and contributes to increased vulnerability in T2D.

Oxidative stress is a defining feature of stroke pathology, but the magnitude, timing and impact of redox imbalance are not static. Emerging evidence indicates that physiological contexts, such as aging, metabolic stress, and circadian disruption, continuously reshape oxidative status and determine the brain's vulnerability to ischemic and reperfusion injury. This review integrates recent insights into how these intrinsic modulators govern the transition from adaptive physiological redox signaling to pathological oxidative stress during stroke. Aging compromises mitochondrial quality control and blunts NRF2-driven antioxidant responses, heightening susceptibility to ROS-driven damage. Metabolic dysfunction, as seen in obesity and diabetes, amplifies oxidative burden through NADPH oxidase activation, lipid peroxidation, and impaired glutathione recycling, further aggravating post-ischemic inflammation. Circadian misalignment, meanwhile, disrupts the rhythmic expression of antioxidant enzymes and metabolic regulators such as BMAL1, REV-ERBα, and SIRT1, constricting the brain's temporal window of resilience. We highlight convergent signaling hubs, NRF2/KEAP1, SIRT-PGC1α, and AMPK pathways, as integrators of these physiological inputs that collectively calibrate redox homeostasis. Recognizing oxidative stress as a dynamic, context-dependent process reframes it from a static pathological state to a dynamic outcome of systemic and temporal imbalance, offering new opportunities for time-sensitive and metabolism-informed redox interventions in stroke.

Resveratrone is a novel compound that was inadvertently discovered by photo-conversion of natural compound resveratrol. Although resveratrol, a representative antioxidant and anti-aging compound, is widely used to promote human health, the benefits of resveratrone have been little studied and remain largely unknown. Since resveratrone has a completely different molecular structure from resveratrol, it has a high possibility of possessing different effects to resveratrol. In this study, the various effects of resveratrone on skin health were revealed, including outstanding antioxidants, whitening, anti-wrinkle, skin regeneration, anti-acne, and so on. Moreover, resveratrone has been confirmed to be an excellent ingredient for skin health because it shows higher performance than resveratrol in most areas.

ROS derived from NADPH oxidase, particularly NOX2, are central to antimicrobial defense, coupling direct pathogen killing with redox signaling that shapes inflammation. This narrative review integrates recent advances on NOX2 structure, assembly, and spatiotemporal control in phagocytes, and outlines how ROS interact with NF-κB, MAPK, and Nrf2 networks to coordinate microbicidal activity and immune modulation. We summarize evidence that both ROS deficiency, as in chronic granulomatous disease, and uncontrolled excess, as in sepsis and severe COVID-19, drive clinically significant pathology, emphasizing the need for precise redox balance. Emerging therapeutic strategies include selective NOX2 inhibitors that limit pathological oxidative bursts, redox-modulating peptides that disrupt upstream activation cues, and Nrf2 activators that enhance endogenous antioxidant capacity, with attention to dosing challenges that preserve host defense while mitigating tissue injury. Key gaps remain in biomarker standardization, real-time in vivo ROS monitoring, and translation from animal models to patients, motivating personalized, combination approaches to redox medicine in infectious diseases.

A high-purity alkaloid-enriched extract (NPAE) was developed from Nelumbinis Plumula. Beyond quantifying its representative alkaloids and total alkaloid content, this study revealed the novel radioprotective role of NPAE against radiation-induced oxidative stress in human umbilical vein endothelial cells (HUVECs). Pretreatment with NPAE significantly attenuated H₂O₂-induced oxidative stress and suppressed irradiation-induced pyroptosis, primarily through restoration of redox homeostasis and inhibition of inflammasome activation. Mechanistic investigations showed that NPAE downregulated the expression of GSDMD-N and cleaved caspase-1, while reducing the secretion of proinflammatory cytokines (IL-18 and IL-1β). These results demonstrate that NPAE effectively alleviates oxidative damage and prevents pyroptosis in endothelial cells, highlighting its potential as a promising phytotherapeutic agent for protection against ionizing radiation injury.

Symphytum officinale L. (Boraginaceae) is a plant with proven anti-inflammatory and analgesic activity on the musculoskeletal system. The traditional use of comfrey primarily refers to its roots, although some literature also mentions the leaves as an alternative plant material. Comparing the therapeutic potential of both plant materials requires additional data on the chemical composition of S. officinale leaves and their biological properties. The aim of the study was to analyze polyphenols in comfrey leaves of different origins and to assess their antioxidant and anti-inflammatory potential against comfrey roots, also collected from different sources. Polyphenol profiles were recognized by 2D TLC and HPLC-DAD-ESI-MS methods, and quantitative analysis was performed by the HPLC-UV/Vis (high performance liquid chromatograph with-ultraviolet/visible detection) method. The antioxidant activity was assessed using DPPH (2,2-diphenyl-1-picrylhydrazyl), FRAP (ferric reducing antioxidant power), and ABTS (2,2'-azino-bis(3-ethylbenzothiazoline- 6-sulfonic acid) diammonium salt) assays, and for leaves also using the TLC-DB (thin layer chromatography-direct bioautography) technique with the DPPH radical. Chemometric analysis to assess the relationship between the antioxidant activity and the origin of comfrey plant raw materials was performed. Factor analysis (FA) confirmed that geographic origin and cultivation conditions influenced the antioxidant content of both plant raw materials. The study results indicate that comfrey leaves can substitute for comfrey roots containing not only caffeic acid derivatives but also flavonoids, and exhibiting stronger antioxidant activity.

Leber's hereditary optic neuropathy (LHON) is a mitochondrial disorder that causes visual impairment due to the degeneration of retinal ganglion cells. Oxidative stress (OS) and inflammatory cytokines have been implicated in its pathophysiology. We investigated, for the first time, the presence of OS biomarkers and inflammatory cytokines in the aqueous humor and peripheral blood of LHON patients compared to controls, aiming to identify potential clinical biomarkers for diagnosis and disease monitoring. A total of 38 participants were enrolled in a single-center, retrospective observational study, including 17 genetically confirmed LHON patients from different Spanish regions and 21 controls. OS biomarkers and inflammatory cytokines were quantified using spectrophotometry and fluorimetry techniques. Statistical analyses were performed to compare groups and to assess the discriminatory performance of biomarkers in identifying affected individuals. Compared to controls, LHON patients exhibited significantly higher levels of AOPP, LOOH, nitrotyrosine, GPX, GRD, and OX/AntiOX ratio in both aqueous humor and serum. Among these, serum LOOH levels and the OX/AntiOX ratio were the most reliable for identifying patients affected, with high sensitivity and specificity. However, additional data on serum IL-1ra are required to confirm its potential as an effective classifier. These findings highlight novel candidate biomarkers for the diagnosis and monitoring of LHON progression.