Modulation Of Oxidative Stress Research Articles

Investigating the Role of Oxidative Stress and Immune Response in Rheumatoid Arthritis

Background:Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune sickness characterized with the aid of persistent joint infection, leading to joint damage and useful impairment. The pathogenesis of RA is thought to be encouraged with the aid of each genetic and environmental elements, with immune device dysregulation playing a valuable role in ailment progression. Increasing proof shows that oxidative pressure, which results from an imbalance between reactive oxygen species (ROS) and antioxidant defenses, contributes to the inflammatory techniques and tissue harm seen in RA. Objectives: This take a look at aimed to investigate the relationship among oxidative pressure and immune machine dysregulation inside the pathogenesis and progression of rheumatoid arthritis (RA). Methodology:This look at turned into conducted from 1st April to 30 November 2024 and protected a total of 200 participants were covered inside the examiner, along with 150 RA patients (75 male and 75 female) and 50 wholesome controls (25 male and 25 lady). The individuals’ ages ranged from 35 to 75 years. Blood samples were collected from the outpatient clinics at Tikrit Teaching Hospital among April and October 2024, and RA patients have been identified primarily based on medical criteria with the aid of the attending physicians. Oxidative strain markers, along with malondialdehyde (MDA) and glutathione (GSH), and pro-inflammatory cytokines, together with IL-1β, IL-17, and TNF-α, had been measured. Disease interest became assessed the usage of the Disease Activity Score 28 (DAS28). Results:The effects revealed that each male and female RA patients had extensively higher levels of MDA and decrease GSH tiers compared to the healthy manage institution. Moreover, seasoned-inflammatory cytokines (IL-1β, IL-17, and TNF-α) had been appreciably improved in RA sufferers, indicating a country of chronic infection. The DAS28 ratings confirmed that a majority of the RA patients had moderate to excessive disorder hobby. No good sized gender-based variations have been discovered in oxidative strain markers, cytokine stages, or sickness interest rankings. Conclusions: Our take a look at highlights the essential interaction among oxidative strain and immune dysregulation in RA. The determined correlations among oxidative markers, pro-inflammatory cytokines, and disease severity underscore the capability for focused on these pathways inside the management of RA. Future studies are warranted to in addition explore the healing ability of antioxidant-primarily based and anti-cytokine treatments in ameliorating RA-associated inflammation and joint damage. Further research is needed to explore the underlying mechanisms and capacity treatments focused on oxidative stress and immune modulation in RA.

Investigating the Role of Oxidative Stress and Immune Response in Rheumatoid Arthritis

Background:Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune sickness characterized with the aid of persistent joint infection, leading to joint damage and useful impairment. The pathogenesis of RA is thought to be encouraged with the aid of each genetic and environmental elements, with immune device dysregulation playing a valuable role in ailment progression. Increasing proof shows that oxidative pressure, which results from an imbalance between reactive oxygen species (ROS) and antioxidant defenses, contributes to the inflammatory techniques and tissue harm seen in RA. Objectives: This take a look at aimed to investigate the relationship among oxidative pressure and immune machine dysregulation inside the pathogenesis and progression of rheumatoid arthritis (RA). Methodology:This look at turned into conducted from 1st April to 30 November 2024 and protected a total of 200 participants were covered inside the examiner, along with 150 RA patients (75 male and 75 female) and 50 wholesome controls (25 male and 25 lady). The individuals’ ages ranged from 35 to 75 years. Blood samples were collected from the outpatient clinics at Tikrit Teaching Hospital among April and October 2024, and RA patients have been identified primarily based on medical criteria with the aid of the attending physicians. Oxidative strain markers, along with malondialdehyde (MDA) and glutathione (GSH), and pro-inflammatory cytokines, together with IL-1β, IL-17, and TNF-α, had been measured. Disease interest became assessed the usage of the Disease Activity Score 28 (DAS28). Results:The effects revealed that each male and female RA patients had extensively higher levels of MDA and decrease GSH tiers compared to the healthy manage institution. Moreover, seasoned-inflammatory cytokines (IL-1β, IL-17, and TNF-α) had been appreciably improved in RA sufferers, indicating a country of chronic infection. The DAS28 ratings confirmed that a majority of the RA patients had moderate to excessive disorder hobby. No good sized gender-based variations have been discovered in oxidative strain markers, cytokine stages, or sickness interest rankings. Conclusions: Our take a look at highlights the essential interaction among oxidative strain and immune dysregulation in RA. The determined correlations among oxidative markers, pro-inflammatory cytokines, and disease severity underscore the capability for focused on these pathways inside the management of RA. Future studies are warranted to in addition explore the healing ability of antioxidant-primarily based and anti-cytokine treatments in ameliorating RA-associated inflammation and joint damage. Further research is needed to explore the underlying mechanisms and capacity treatments focused on oxidative stress and immune modulation in RA.

Effects of Wildfire Exposure on the Human Immune System

Wildfires have become a significant environmental and public health concern worldwide, particularly due to their increased frequency and intensity driven by climate change. Wildfire smoke, composed of a complex mixture of particulate matter, gases and chemicals, has been linked to numerous health issues, primarily affecting the respiratory and cardiovascular systems. However, emerging evidence suggests that wildfire smoke exposure also has profound effects on the immune system. This review aims to synthesize current knowledge on how wildfire smoke exposure affects the human immune system, including acute and chronic impacts, underlying mechanisms and potential long-term consequences. The review discusses the role of inflammation, oxidative stress and immune cell modulation in response to wildfire smoke, highlighting the need for further research to fully understand these effects.

Impact of DPP-4 Inhibitors in Patients with Diabetes Mellitus and Heart Failure: An In-Depth Review

The increasing prevalence of both type 2 diabetes mellitus and heart failure has underscored the urgent need for optimized therapeutic strategies that address the complex interplay between these conditions. Dipeptidyl peptidase-4 (DPP-4) inhibitors have emerged as a popular class of glucose-lowering agents due to their favorable glycemic effects, safety profile, and potential cardiovascular benefits. However, the impact of DPP-4 inhibitors on heart failure outcomes in patients with diabetes remains contentious, with conflicting evidence from clinical trials and observational studies. This review critically examines current evidence on the use of DPP-4 inhibitors in patients with coexisting diabetes and heart failure, focusing on pharmacodynamics, safety, and efficacy outcomes. We explore the physiological mechanisms by which DPP-4 inhibitors may influence heart failure risk, including modulation of inflammation, oxidative stress, and myocardial fibrosis. Clinical trials such as SAVOR-TIMI 53, EXAMINE, and TECOS are evaluated to provide a comprehensive analysis of DPP-4 inhibitors’ effects on hospitalization for heart failure, mortality, and cardiovascular events in diabetic patients. While some trials suggest an increased risk of HF hospitalizations with specific DPP-4 inhibitors (e.g., saxagliptin), others report neutral effects, raising questions about the class effects versus individual drug characteristics within this group. Additionally, we address discrepancies in outcomes related to patient demographics, HF phenotype, and comorbid conditions that may influence DPP-4 inhibitors’ risk–benefit profile. Comparative insights into alternative glucose-lowering therapies such as SGLT2 inhibitors and GLP-1 receptor agonists are also provided, highlighting potential implications for treatment selection in this high-risk population. In summary, this review synthesizes available evidence on DPP-4 inhibitors’ impact in diabetic patients with heart failure, aiming to guide clinicians in making informed therapeutic decisions. While DPP-4 inhibitors remain a viable option in diabetes management, caution is warranted in patients with advanced heart failure, and future research is essential to refine patient-specific guidelines.

Targeted delivery of a selenium-sulfa compound via cationic starch microparticles: Modulation of oxidative stress and pain pathways in fibromyalgia-like symptoms in mice

Cationic starch microparticles (CStMPs) loaded with 4-amino-3 -(phenylselenyl)benzenesulfonamide (4-APSB) were prepared and investigated in a model of fibromyalgia (FM) induced by intermittent cold stress (ICS) in male and female Swiss mice. The CStMPs/4-APSB were characterized by Fourier transform infrared (FTIR) spectroscopy, scanning electron microscopy (SEM), energy-dispersive X-ray (EDX) spectroscopy, zeta potential, and particle size measurements, providing information about their chemical composition, surface charge, morphology/microstructure, and size (1.50 ± 0.5 μm). Following ICS exposure, the animals were treated with free 4-APSB (1 mg/kg), CStMPs/4-APSB (containing 0.13 mg of 4-APSB per mg of microparticles), or CStMPs, from days 5 to 10. The results revealed the successful incorporation of 4-APBS in the CStMPs. Free 4-APSB and CStMPs/4-APSB reversed nociceptive- and depressive-related behaviors in male and female mice exposed to ICS, attenuating the hallmark symptoms of FM. Those treatments (free 4-APSB and CStMPs/4-APSB) normalized the monoamine oxidase (MAO)-A activity in the cerebral cortex and the oxidative damage, providing the correct functioning of the enzyme Ca2+ -ATPase in the cerebral cortex and hippocampus of mice exposed to ICS. The CStMPs/4-APSB modulated the oxidative stress markers, specifically in the spinal cord of mice - an anatomical region intricately linked to pain pathways.

МИКРОБИОТА КИШЕЧНИКА И ЗДОРОВЬЕ СПОРТСМЕНОВ

Purpose: A synthesis of world literature on actual knowledge of intestine microbiota influence on athletes’ health. Methods and materials: National and foreign literature on actual knowledge of intestine microbiota influence on athletes’ health was analyzed. MEDLINE, Embase, Scopus, Web of Science, eLIBRARY, PubMed data Google Academy data bases were used for searching the literature for the period from 2012 to 2024. The following key words and their combinations were applied for search: “athletes”, “gut microbiota “, “butyrate”. Results: A microbiota is a key factor of human organism homeostasis maintenance. It provides next functions: energy metabolism, maturation and maintenance of immune system, synthesis of vitamins, regulation of bile acids reabsorption in intestine and lots of other functions. Furthermore, bacteria produce some human hormones analogues: serotonin, histamine, dopamine, norepinephrine, testosterone. According to the recent information, intestine microbiota modification could provide a beneficial influence on human organism that cause a sport results improvement. Modulation of immune response, oxidative stress, metabolic processes and nutrients bioavailability is a general mechanism of microbiota influence on training adaptation. Microbiome affects the muscular protein synthesis, biogenesis and function of mitochondria and the muscular glycogen accumulation. Conclusion: Currently there is a necessity of further investigations of “microbiome-muscles” relationship.

Insights on the Genetic and Phenotypic Complexities of Optic Neuropathies

Background/Objectives: Optic neuropathies are a category of illnesses that ultimately cause damage to the optic nerve, leading to vision impairment and possible blindness. Disorders such as dominant optic atrophy (DOA), Leber hereditary optic neuropathy (LHON), and glaucoma demonstrate intricate genetic foundations and varied phenotypic manifestations. This narrative review study seeks to consolidate existing knowledge on the genetic and molecular mechanisms underlying ocular neuropathies, examine genotype-phenotype correlations, and assess novel therapeutic options to improve diagnostic and treatment methodologies. Methods: A systematic literature review was performed in October 2024, utilizing PubMed, Medline, the Cochrane Library, and ClinicalTrials.gov. Search terms encompassed “optic neuropathy”, “genetic variants”, “LHON”, “DOA”, “glaucoma”, and “molecular therapies”. Studies were chosen according to established inclusion criteria, concentrating on the genetic and molecular dimensions of optic neuropathies and their therapeutic ramifications. Results: The results indicate that DOA and LHON are mostly associated with the mitochondrial dysfunction resulting from pathogenic variants in nuclear genes, mainly OPA1, and mitochondrial DNA (mtDNA) genes, respectively. Glaucoma, especially its intricate variants, is linked to variants in genes like MYOC, OPTN, and TBK1. Molecular mechanisms, such as oxidative stress and inflammatory modulation, are pivotal in disease progression. Innovative therapeutics, including gene therapy, RNA-based treatments, and antioxidants such as idebenone, exhibit promise for alleviating optic nerve damage and safeguarding vision. Conclusions: Genetic and molecular investigations have markedly enhanced our comprehension of ocular neuropathies. The amalgamation of genetic and phenotypic data is essential for customized medical strategies. Additional research is required to enhance therapeutic strategies and fill the gaps in our understanding of the underlying pathophysiology. This interdisciplinary approach shows potential for enhancing patient outcomes in ocular neuropathies.

The Role of Trace Elements in COPD: Pathogenetic Mechanisms and Therapeutic Potential of Zinc, Iron, Magnesium, Selenium, Manganese, Copper, and Calcium.

Chronic obstructive pulmonary disease (COPD) is a progressive, inflammatory airway disorder characterized by a gradual decline in lung function and increased oxidative stress. Both oxidative stress and inflammation are central to its pathophysiology, with trace elements such as zinc, copper, iron, manganese, magnesium, selenium, and calcium playing key roles in various cellular processes. This article reviews the role of trace elements in COPD, focusing on their involvement in disease pathogenesis and their therapeutic potential. Specifically, we examine the effects of zinc, copper, iron, magnesium, manganese, selenium, and calcium in COPD. We performed a comprehensive narrative review of the literature across databases including PubMed, Web of Science, Cochrane Library, and Google Scholar, identifying studies that explore the therapeutic effects of trace elements in COPD. The studies included in the review consisted of cohort analyses, randomized controlled trials, and clinical investigations. Zinc, copper, iron, magnesium, manganese, selenium, and calcium are critical to both the pathophysiology and management of COPD. These trace elements contribute to the regulation of inflammation, the modulation of oxidative stress, and the maintenance of lung function. Zinc and copper, for instance, reduce oxidative stress and modulate immune responses, while iron is essential for oxygen transport. Magnesium, manganese, selenium, and calcium are vital for muscle function, respiratory performance, reducing inflammation, and improving pulmonary function. The minerals zinc, copper, iron, magnesium, manganese, selenium, and calcium may contribute to beneficial effects as part of the standard therapeutic management of COPD. Maintaining optimal levels of these trace elements may support the regulation of inflammatory processes, a reduction in oxidative stress, and an improvement in the pulmonary function. However, further clinical research is necessary to confirm their efficacy and establish safe dosage recommendations in COPD treatment.

Polyphenols and Functionalized Hydrogels for Osteoporotic Bone Regeneration.

Osteoporosis induces severe oxidative stress and disrupts bone metabolism, complicating the treatment of bone defects. Current therapies often have side effects and require lengthy bone regeneration periods. Hydrogels, known for their flexible mechanical properties and degradability, are promising carriers for drugs and bioactive factors in bone tissue engineering. However, they lack the ability to regulate the local pathological environment of osteoporosis and expedite bone repair. Polyphenols, with antioxidative, anti-inflammatory, and bone metabolism-regulating properties, have emerged as a solution. Combining hydrogels and polyphenols, polyphenol-based hydrogels can regulate local bone metabolism and oxidative stress while providing mechanical support and tissue adhesion, promoting osteoporotic bone regeneration. This review first provides a brief overview of the types of polyphenols and the mechanisms of polyphenols in facilitating adhesion, antioxidant, anti-inflammatory, and bone metabolism modulation in modulating the pathological environment of osteoporosis. Next, this review examines recent advances in hydrogels for the treatment of osteoporotic bone defects, including their use in angiogenesis, oxidative stress modulation, drug delivery, and stem cell therapy. Finally, it highlights the latest research on polyphenol hydrogels in osteoporotic bone defect regeneration. Overall, this review aims to facilitate the clinical application of polyphenol hydrogels for the treatment of osteoporotic bone defects.

A Review on the Protecting Effects and Molecular Mechanisms of Berries Against a Silent Public Health Concern: Non-Alcoholic Fatty Liver Disease.

Non-alcoholic fatty liver disease (NAFLD) poses a silent threat to human health, with prevalence rising at an alarming rate. The treatment and prevention of NAFLD depend on novel approaches as no effective treatment options are currently available. Berries are unique sources of phenolic compounds that have proven roles in disease prevention and health promotion. However, a comprehensive review of the effects of different berries on NAFLD and related pathologies is lacking. Thus, the present review aims to summarize the effects of berry extracts, plant parts, and bioactive compounds from twenty-one different berries on NAFLD. The molecular mechanisms involved include the regulation of lipid homeostasis, modulation of oxidative stress and inflammation markers, and activation of different signaling pathways in different in vitro and in vivo NAFLD models. Furthermore, their modulatory effects on the gut microbiota have also been highlighted. Clinical intervention research on the benefits of berries in NAFLD is limited; nonetheless, this paper discusses clinical studies demonstrating the effects of different berries in people with NAFLD. Future research should focus on long-term clinical studies to compare the therapeutic potentials of different berries against NAFLD.

Gut Microbiota and Metabolic Dysfunction-Associated Steatotic Liver Disease.

Background: The gut microbiota constitutes a complex microorganism community that harbors bacteria, viruses, fungi, protozoa, and archaea. The human gut bacterial microbiota has been extensively proven to participate in human metabolism, immunity, and nutrient absorption. Its imbalance, namely "dysbiosis", has been linked to disordered metabolism. Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the features of deranged human metabolism and is the leading cause of liver cirrhosis and hepatocellular carcinoma. Thus, there is a pathophysiological link between gut dysbiosis and MASLD. Aims and Methods: We aimed to review the literature data on the composition of the human bacterial gut microbiota and its dysbiosis in MASLD and describe the concept of the "gut-liver axis". Moreover, we reviewed the approaches for gut microbiota modulation in MASLD treatment. Results: There is consolidated evidence of particular gut dysbiosis associated with MASLD and its stages. The model explaining the relationship between gut microbiota and the liver has a bidirectional organization, explaining the physiopathology of MASLD. Oxidative stress is one of the keystones in the pathophysiology of MASLD and fibrosis generation. There is promising and consolidated evidence for the efficacy of pre- and probiotics in reversing gut dysbiosis in MASLD patients, with therapeutic effects. Few yet encouraging data on fecal microbiota transplantation (FMT) in MASLD are available in the literature. Conclusions: The gut dysbiosis characteristic of MASLD is a key target in its reversal and treatment via diet, pre/probiotics, and FMT treatment. Oxidative stress modulation remains a promising target for MASLD treatment, prevention, and reversal.

Chlorogenic acid improves urogenital dysfunction induced by exposure to ambient particulate matter.

Oxidative stress is a well-known underlying mechanism for several diseases in response to environmental pollution. Although there is a lack of evidence on the relationship between air pollution and an established risk factor for urogenital dysfunction. The aim of this study was to investigate the mechanism of particulate matter (PM) on urogenital function and evaluate the potential efficacy of chlorogenic acid (CGA) in preventing urogenital damage in rats. Forty Wistar rats were divided into five groups (n = 8): control, particulate matter exposure (animals were exposed to fine dust in an inhalation chamber for 4 weeks, 3 days a week, for 3 h, PM10 concentration adjusted to 500-2000 µg/m3), and particulate matter plus 3 concentrations of chlorogenic acid (100, 200, and 400 mg/kg, gavage, 4 weeks, 3 days a week). At the end of the study, kidney biomarkers, oxidative stress markers, antioxidant enzymes, the oxidation resistance 1 (OXR1) and its downstream gene expression, sperm count, gonadotropin hormones, and the structure of the kidney, epididymis, and seminal vesicle were evaluated in response to PM exposure and CGA treatment in all groups. The data obtained from the current study showed that PM exposure led to kidney dysfunction and inhibition of oligospermia through oxidative stress, as evidenced by an increase in MDA and a decrease in TAC, SOD, CAT, and GSH concentration levels in blood samples. These results were consistent with the down-regulation of OXR1, Nrf2, and P21 gene expression. In contrast, CGA improved urogenital biomarkers and histopathology structures of the kidney, epididymis, and seminal vesicle by enhancing antioxidant defense system enzymes and modulating the OXR1 signaling pathway. Our findings suggest that environmental air pollution contributes to kidney dysfunction and urogenital damage. Modulation of oxidative stress through the OXR1, P21, and Nrf2 signaling pathways may be the underlying mechanism. Furthermore, chlorogenic acid supplementation could be recommended as a new protective or treatment strategy to safeguard urogenital function against exposure to particulate matter.

Renoprotective Effects of Brown-Strain Flammulina velutipes Singer in Chronic Kidney Disease-Induced Mice Through Modulation of Oxidative Stress and Inflammation and Regulation of Renal Transporters.

Cisplatin, widely used in chemotherapy, acts through mechanisms such as oxidative stress to damage the DNA and cause the apoptosis of cancer cells. Although effective, cisplatin treatment is associated with considerable side effects including chronic kidney disease (CKD). Studies on brown-strain Flammulina velutipes Singer (FVB) have shown its significant antioxidant and immunomodulatory effects. High-performance liquid chromatography (HPLC) confirmed that the FVB extract contained gallic acid and quercetin. This study investigated whether FVB extract can improve and protect against cisplatin-induced CKD in mice. C57BL/6 mice were used as an animal model, and CKD was induced through intraperitoneal cisplatin injection. FVB was orally administered to the mice for 14 consecutive days. N-acetylcysteine (NAC) was administered in the positive control group. Organ pathology and serum biochemical analyses were conducted after the mice were sacrificed. Significant dose-dependent differences were discovered in body mass, kidney mass, histopathology, renal function, inflammatory factors, and antioxidant functions among the different groups. FVB extract reduced the severity of cisplatin-induced CKD in pathways related to inflammation, autophagy, apoptosis, fibrosis, oxidative stress, and organic ion transport proteins; FVB extract, thus, displays protective physiological activity in kidney cells. Additionally, orally administered high doses of the FVB extract resulted in significantly superior renal function, inflammatory factors, antioxidative activity, and fibrotic pathways. This study establishes a strategy for future clinical adjunctive therapy using edible-mushroom-derived FVB extract to protect kidney function.

Herbo-vitamin medicine Livogrit Vital ameliorates isoniazid induced liver injury (IILI) in human liver (HepG2) cells by decreasing isoniazid accumulation and oxidative stress driven hepatotoxicity

BackgroundTuberculosis (TB) is a leading cause of infection related mortality. Isoniazid is one of the frontline drugs for anti-TB therapy. Hepatotoxicity induced by isoniazid is a major cause of drug-discontinuation which may lead to development of resistant TB or increased mortality.PurposeTo characterize pharmacological properties of plant-based prescription medicine, Livogrit Vital (LVV) against isoniazid-induced liver injury (IILI) using HepG2 cells.MethodPhytometabolite characterization of LVV was performed by High-performance liquid chromatography (HPLC). The effects of LVV on cytosafety, IC50 shift, oxidative stress, ER stress, apoptosis, liver injury markers, and accumulation of isoniazid and hydrazine was performed on HepG2 cells induced with isoniazid. Silymarin was used as the positive control.ResultsHPLC based phytometabolite characterization of LVV revealed the presence of several anti-oxidant, anti-apoptotic, and hepatoprotective compounds. In isoniazid-induced HepG2 cells, LVV reduced cytotoxicity of isoniazid and shifted its IC50 value. Treatment with LVV reduced ROS generation and lipid peroxidation; enhanced GSH enzyme levels in isoniazid-induced HepG2 cells. As per the mechanistic evaluation, LVV modulated gene expression level of Caspase-3, FGF21, and IRE-1α. LVV treatment also normalized isoniazid-induced elevated Caspase-3 activity and cPARP1 protein levels, indicating its potentials to regulate liver cell apoptosis. Concomitantly, biomarkers of hepatotoxicity, ALT and GGT, also decreased by LVV treatment. Interestingly, LVV treatment reduced intracellular accumulation of isoniazid and its toxic metabolite hydrazine, in isoniazid-stimulated HepG2 cells.ConclusionTreatment of hepatic cells with the herbo-vitamin medicine, Livogrit Vital, regulates IILI by modulation of oxidative and ER stress, apoptosis, and bioaccumulation of isoniazid and hydrazine. Collectively, Livogrit Vital could well be explored as an adjuvant hepatoprotective agent alongwith anti-TB medicines.

Mitigation of streptozotocin-induced diabetic nephropathy in rats through the modulation of hyperlipidemia, oxidative stress, and inflammatory markers by nicotinamide in combination with selenium nanoparticles

Mitigation of streptozotocin-induced diabetic nephropathy in rats through the modulation of hyperlipidemia, oxidative stress, and inflammatory markers by nicotinamide in combination with selenium nanoparticles

Neuroprotective Potential of Glycyrrhizic Acid in Ischemic Stroke: Mechanisms and Therapeutic Prospects.

Background/Objectives: Ischemic stroke is a leading cause of disability and mortality worldwide, with current therapies limited in addressing its complex pathophysiological mechanisms, such as inflammation, oxidative stress, apoptosis, and impaired autophagy. Glycyrrhizic acid (GA), a bioactive compound from licorice (Glycyrrhiza glabra L.), has demonstrated neuroprotective properties in preclinical studies. This review consolidates current evidence on GA's pharmacological mechanisms and assesses its potential as a therapeutic agent for ischemic stroke. Methods: This review examines findings from recent preclinical studies and reviews on GA's neuroprotective effects, focusing on its modulation of inflammation, oxidative stress, apoptosis, and autophagy. Studies were identified from major scientific databases, including PubMed, Web of Science, and Embase, covering research from January 2000 to August 2024. Results: GA has demonstrated significant neuroprotective effects through the modulation of key pathways, including HMGB1/TLR4/NF-κB and Keap1/Nrf2, thereby reducing neuroinflammation, oxidative stress, and apoptosis. Additionally, GA promotes autophagy and modulates immune responses, suggesting it could serve as an adjunct therapy to enhance the efficacy and safety of existing treatments, such as thrombolysis. Conclusions: Current findings underscore GA's potential as a multi-targeted neuroprotective agent in ischemic stroke, highlighting its anti-inflammatory, antioxidant, and anti-apoptotic properties. However, while preclinical data are promising, further clinical trials are necessary to validate GA's therapeutic potential in humans. This review provides a comprehensive overview of GA's mechanisms of action, proposing directions for future research to explore its role in ischemic stroke management.

Probiotic, Postbiotic, and Paraprobiotic Effects of Lactobacillus rhamnosus as a Modulator of Obesity-Associated Factors.

Obesity is a pandemic currently affecting the world's population that decreases the quality of life and promotes the development of chronic non-communicable diseases. Lactobacillus rhamnosus is recognized for multiple positive effects on obesity and overall health. In fact, such effects may occur even when the microorganisms do not remain alive (paraprobiotic effects). This raises the need to elucidate the mechanisms by which obesity-associated factors can be modulated. This narrative review explores recent findings on the effects of L. rhamnosus, particularly, its postbiotic and paraprobiotic effects, on the modulation of adiposity, weight gain, oxidative stress, inflammation, adipokines, satiety, and maintenance of intestinal integrity, with the aim of providing a better understanding of its mechanisms of action in order to contribute to streamlining its clinical and therapeutic applications. The literature shows that L. rhamnosus can modulate obesity-associated factors when analyzed in vitro and in vivo. Moreover, its postbiotic and paraprobiotic effects may be comparable to the more studied probiotic actions. Some mechanisms involve regulation of gene expression, intracellular signaling, and enteroendocrine communication, among others. We conclude that the evidence is promising, although there are still multiple knowledge gaps that require further study in order to fully utilize L. rhamnosus to improve human health.

Therapeutic potential of plant polyphenols in acute pancreatitis.

Acute pancreatitis is a potentially life-threatening inflammatory disorder of the exocrine pancreas characterized by early activation of pancreatic enzymes followed by macrophage-driven inflammation, and pancreatic acinar cell death. The most common causes are gallstones and excessive alcohol consumption. Inflammation and oxidative stress play critical roles in its pathogenesis. Despite increasing incidence, currently, no specific drug therapy is available to treat or prevent acute pancreatitis, in particular severe acute pancreatitis. New therapeutic agents are very much needed. Plant polyphenols have attracted extensive attention in the field of acute pancreatitis due to their diverse pharmacological properties. In this review, we discuss the potential of plant polyphenols in inhibiting the occurrence and development of acute pancreatitis via modulation of inflammation, oxidative stress, calcium overload, autophagy, and apoptosis, based on the currently available in vitro, in vivo animal and very few clinical human studies. We also outline the opportunities and challenges in the clinical translation of plant polyphenols for the treatment of the disease. We concluded that plant polyphenols have a potential therapeutic effect in the management and treatment of acute pancreatitis. Knowledge gained from this review will hopefully inspire new research ideas and directions for the development and application of plant polyphenols for treating this disease.

Effects of Resveratrol on Nonmelanoma Skin Cancer (NMSC): A Comprehensive Review.

Nonmelanoma skin cancer (NMSC) represents the most prevalent form of skin cancer globally, with basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) being the most common types. The search for effective chemopreventive and therapeutic agents has led to the exploration of natural compounds, among which resveratrol (RES), a polyphenolic phytoalexin found in grapes, berries, peanuts, and red wine, has garnered significant attention. This comprehensive review aims to elucidate the effects of RES on NMSC, focusing on its mechanisms of action, efficacy in preclinical studies, and potential as a chemopreventive and therapeutic agent. RES exhibits promising chemopreventive and antineoplastic capabilities against NMSC through various mechanisms, including the induction of apoptosis, inhibition of cell proliferation, modulation of oxidative stress, and anti-inflammatory activities. Studies have demonstrated that RES can significantly enhance the effectiveness of traditional chemotherapeutic agents, such as 5-fluorouracil (5-FU), by inhibiting cellular proliferation and inducing apoptosis in cancerous cells. Furthermore, resveratrol's antioxidant properties may mitigate the impact of reactive oxygen species (ROS) triggered by UV exposure, thus reducing DNA damage and mutations associated with skin cancer development. Invitro and invivo experiments have shown that RES can effectively hinder the growth and spread of various tumor cell types, including human cutaneous SCC A431 cells, and induce apoptosis. The development of advanced delivery systems, such as nanostructured lipid carriers and liposomes, has been recognized for their potential to enhance the therapeutic effects of RES, particularly its anticancer properties. In conclusion, RES presents a viable candidate for the prevention and treatment of NMSC, owing to its multifaceted mechanisms of action, including its ability to regulate oxidative stress, trigger apoptosis, and inhibit proliferation. However, further clinical studies are required to fully understand its effectiveness and safety in humans, as well as to optimize delivery methods for improved bioavailability and therapeutic outcomes.

Polyphenol Enhances the Functionality of Borate Hydrogel in Wound Repair by Regulating the Wound Microenvironment

Wound infections represent a significant clinical challenge. In this study, a polyphenol (tannic acid, TA)-enhanced borate hydrogel modulating the tissue microenvironment to promote wound healing was designed as an antimicrobial hydrogel. The physical properties of the multiply cross-linked borate hydrogel were analyzed using a combination of techniques, including FT-IR, 1H NMR, SEM, and rheological analysis. The combination of polyvinyl alcohol (PVA), phenylboronic acid-functionalized chitosan (N-PBACS), and TA resulted in the formation of multi-crosslinked networks (PVA@N-PBACS, TA@PVA, and TA@N-PBACS) that markedly enhanced the hydrogel's mechanical strength, deformability (compression and tensile), and adhesion properties. The multi-crosslinked hydrogels exhibited broad-spectrum antimicrobial activity and antioxidant effects in vitro, as well as excellent biocompatibility and the promotion of cell proliferation, migration and vascularisation behaviours. The in vivo results demonstrated that the hydrogel had enhanced properties. Furthermore, it exhibits good biocompatibility, reactive oxygen species (ROS) scavenging ability, antimicrobial properties, and the ability to modulate immune status. In an in vivo bacterial infection model, the multi-crosslinked hydrogel effectively modulated the wound microenvironment through antimicrobial effects, oxidative stress, ROS levels, and immunity modulation. This study offers a promising solution for improving wound care and provides insight into potential future therapeutic strategies.