Oxidative Stress and Inflammation, 3rd Edition

Topic Information

Dear Colleagues,

Oxidative stress is viewed as an imbalance between the production of reactive oxygen species (ROS) and their elimination by protective mechanisms, which can lead to chronic inflammation. Certain lifestyles and the intake of external unhealthy chemicals are the major causes of age-related chronic diseases and cancer. Their study includes disease pathology pathways, lifestyle, treatment, protection, and prevention of oxidative stress and inflammation. ROS are normally produced within the body in limited amounts and are essential compounds involved in the regulation of processes that can maintain cell homeostasis and functions (signal transduction, gene expression, and activation of receptors). An imbalance may cause oxidative stress, which can lead to lipid peroxidation, gene mutation, inflammation, and other complications. The harmful oxidative activity of ROS can be only counteracted by antioxidant/anti-inflammatory compounds, which may be both synthetic and natural, but are often characterized by several stability issues, such as poor water solubility and low bioavailability, which compromise their in vivo activities. The aim of this Topic is to collect research papers providing an overview of the current status of research on both natural and synthetic products with antioxidant properties that can counteract inflammatory diseases, including, but not necessarily restricted to, chemical compounds (synthetic or of natural origin), vitamins, peptides, micronutrients, non-starch polysaccharides, probiotics, postbiotics, prebiotics formulations containing functional foods, nutraceutical or cosmeceutical products, and innovative oral, systemic, or topical delivery methods that are capable of overcoming their stability issues.

Dr. Maria Letizia Manca
Dr. Amparo Nacher
Dr. Matteo Perra
Dr. Ines Castangia
Dr. Mohamad Allaw
Topic Editors

Keywords

Participating Journals

Journal Name	Impact Factor	CiteScore	Launched Year	First Decision (median)	APC
Antioxidants antioxidants	6.6	12.4	2012	18.7 Days	CHF 2900	Submit
Biomedicines biomedicines	3.9	6.8	2013	21 Days	CHF 2600	Submit
Cosmetics cosmetics	3.2	6.0	2014	20.1 Days	CHF 1800	Submit
International Journal of Molecular Sciences ijms	4.9	9.0	2000	17.8 Days	CHF 2900	Submit
Life life	3.4	6.0	2011	16.6 Days	CHF 2600	Submit
Nutraceuticals nutraceuticals	-	-	2021	21.1 Days	CHF 1200	Submit
Oxygen oxygen	-	8.4	2021	26.7 Days	CHF 1200	Submit

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Published Papers (12 papers)

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Open AccessArticle

Hepatic ACSL4 Loss Boosts Endogenous Gamma-Glutamylcysteine to Alleviate Alcoholic Liver Disease

by Ran Duan, Xin-Yi Wang, Xue Zhou, Jing-Wen Ding, Zhi-Sen Yang, Zhi-Lin Li, Yue-Yu Wang, Jia-Xin Yu and Jing-Jing Duan

Antioxidants 2026, 15(4), 438; https://doi.org/10.3390/antiox15040438 - 31 Mar 2026

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Abstract

Alcoholic liver disease (ALD), secondary to chronic alcohol abuse, encompasses a spectrum of liver disorders that progress from steatosis and hepatitis to fibrosis, cirrhosis, and acute-on-chronic liver failure. It poses a considerable global health burden due to its elevated rates of associated morbidity [...] Read more.

Alcoholic liver disease (ALD), secondary to chronic alcohol abuse, encompasses a spectrum of liver disorders that progress from steatosis and hepatitis to fibrosis, cirrhosis, and acute-on-chronic liver failure. It poses a considerable global health burden due to its elevated rates of associated morbidity and mortality. The rising prevalence of ALD, coupled with the lack of approved pharmacotherapies, presents considerable unmet clinical needs. In this study, long-chain acyl-CoA synthetase 4 (ACSL4) was identified as a pathogenic driver in the context of chronic alcohol consumption. Hepatocyte Acsl4 ablation mitigated key pathological manifestations in Gao-Binge model mice, as evidenced by reduced inflammatory cell infiltration and attenuated lipid accumulation. Mechanistically, ACSL4 inhibition augmented cellular antioxidant defence through elevating gamma-glutamylcysteine (γ-GC) levels. In addition, γ-GC bound to and suppressed the expression of protein tyrosine phosphatase type IVA member 1 (PTP4A1). Both genetic silencing and pharmacological inhibition of PTP4A1 attenuated the activation of the downstream MAPK-NF-κB inflammatory cascade. Dronedarone, identified as a novel compound targeting ACSL4, demonstrated efficacy in ameliorating the progression of ALD. Overall, these findings elucidate a novel mechanism wherein ACSL4 modulates antioxidant responses via a small bioactive peptide, highlighting ACSL4 as a potential therapeutic target for ALD. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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Open AccessArticle

Uric Acid Induces Hepatocytes Ferroptosis Through HIF-2α/DMT1-Mediated Iron Overload

by Tao Wang, Wanbao Zheng, Meimei Guo, Jun Cao, Li Wang, Marco Sim Kah How, Youzhi Xu and Wenjie Lu

Int. J. Mol. Sci. 2026, 27(6), 2833; https://doi.org/10.3390/ijms27062833 - 20 Mar 2026

Viewed by 317

Abstract

Hyperuricemia is associated with liver dysfunction, yet its molecular mechanisms remain unclear. This study investigated high uric acid (HUA)-induced hepatocyte injury using a hyperuricemia mouse model (HUM) and uric acid (UA)-treated L02 cells. HUM exhibited elevated aspartate aminotransferase (AST)/alanine aminotransferase (ALT) and pathological [...] Read more.

Hyperuricemia is associated with liver dysfunction, yet its molecular mechanisms remain unclear. This study investigated high uric acid (HUA)-induced hepatocyte injury using a hyperuricemia mouse model (HUM) and uric acid (UA)-treated L02 cells. HUM exhibited elevated aspartate aminotransferase (AST)/alanine aminotransferase (ALT) and pathological liver changes. Transmission electron microscopy (TEM) confirmed ferroptotic hallmarks, including mitochondrial shrinkage and increased membrane density. UA exposure upregulated NADPH oxidase 4 (NOX4), increased reactive oxygen species (ROS), and promoted lipid peroxidation (LPO), accompanied by intracellular Fe²⁺ accumulation. Mechanistically, UA increased hypoxia-inducible factor-2α (HIF-2α) expression, subsequently upregulating iron transporters divalent metal transporter 1 (DMT1) and transferrin receptor (TFRC). Deferoxamine (DFO) treatment effectively reversed Fe²⁺ overload and alleviated oxidative stress. Notably, pharmacological inhibition or genetic knockdown of HIF-2α specifically suppressed DMT1 upregulation and restored iron homeostasis, while TFRC expression remained unaffected. Blocking the HIF-2α/DMT1 axis significantly reduced LPO and mitochondrial dysfunction. These findings demonstrate that HUA induces hepatocyte ferroptosis through HIF-2α-mediated DMT1 upregulation, leading to Fe²⁺ overload and mitochondrial impairment. This study identifies the HIF-2α/DMT1 pathway as a key driver of HUA-induced liver injury and a potential therapeutic target. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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18 pages, 3179 KB  

Open AccessArticle

Cosmetic Efficacy and Sustainability of Beer and Brewing By-Products in Skin Care: A Formulation-Driven In Vitro and In Vivo Evaluation

by Ela Hoti, Camilla Elena Di Bella, Sabina Hoti, Dolores Vargas Peregrina, Maria Giovanna Sabbieti, Dimitrios Agas, Piera Di Martino, Susi Zara and Maria Rosa Gigliobianco

Cosmetics 2026, 13(2), 63; https://doi.org/10.3390/cosmetics13020063 - 7 Mar 2026

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The brewing process generates substantial by-products rich in potentially bioactive compounds (e.g., polyphenols and fermentation metabolites), providing a sustainable and appealing source of cosmetic ingredients. Oil-in-water (O/W) emulsions containing 20% (w/w) aqueous extracts from Bionda Triplo Malto beer, wort, [...] Read more.

The brewing process generates substantial by-products rich in potentially bioactive compounds (e.g., polyphenols and fermentation metabolites), providing a sustainable and appealing source of cosmetic ingredients. Oil-in-water (O/W) emulsions containing 20% (w/w) aqueous extracts from Bionda Triplo Malto beer, wort, and key brewing by-products (hops, yeast, and spent grain) were developed and evaluated using a combined in vitro–in vivo approach. Aqueous extracts were first screened on human immortalized dermal fibroblasts (BJ-5ta) at 0.25–1 mg/mL for cytocompatibility and antioxidant activity. Within this concentration range, no significant changes in cell viability or intracellular antioxidant capacity under UV stress were detected, suggesting cytocompatibility but limited inherent activity. When incorporated into O/W emulsions and tested at an active-equivalent concentration of 10 mg/mL, the formulations increased fibroblast metabolic activity and antioxidant response. In contrast, free extracts at 10 mg/mL showed concentration-dependent cytotoxicity for some matrices, with beer- and yeast-based emulsions demonstrating the strongest effects. The emulsions exhibited good physicochemical stability (pH ~5.7–6.2; viscosity 4750–5150 mPa·s), passed the ISO 11930:2012 challenge test, and were well tolerated in patch testing. In a double-blind, randomized split-forearm study on 50 healthy volunteers over 30 days, beer, yeast, and spent grain-based formulations improved skin parameters versus baseline. TEWL decreased (e.g., beer: 16.22 ± 5.12 to 10.77 ± 2.22 mg·m⁻²·h⁻¹; yeast: 16.29 ± 5.66 to 10.18 ± 1.08; spent grain: 14.45 ± 4.34 to 11.66 ± 2.28), hydration increased (beer: 35.15 ± 5.93 to 42.26 ± 3.78; yeast: 33.27 ± 4.87 to 42.92 ± 2.48; spent grain: 34.22 ± 5.19 to 41.16 ± 3.17, and elasticity improved for beer and yeast formulations (62.33 ± 3.27 to 70.24 ± 2.12 N/m) and yeast (61.21 ± 4.72 to 72.13 ± 5.55 N/m). Based on these findings, brewing-derived ingredients demonstrate potential as cosmetic actives, with formulation critically determining their clinical efficacy. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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15 pages, 794 KB  

Open AccessArticle

Lipoprotein Combine Index Is Associated with Multi-Compartment Oxidative Stress in Clinically Stable Peritoneal Dialysis Patients: A Cross-Sectional Study

by Natalia Stepanova and Lesya Korol

Biomedicines 2026, 14(2), 456; https://doi.org/10.3390/biomedicines14020456 - 18 Feb 2026

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Background/Objectives: Background: Dyslipidaemia and oxidative stress (OS) are frequent in peritoneal dialysis (PD). The Lipoprotein Combine Index (LCI) integrates lipid parameters, but its relationship with peritoneal transport and OS is unclear. Methods: This cross-sectional study included 100 clinically stable adults on continuous [...] Read more.

Background/Objectives: Background: Dyslipidaemia and oxidative stress (OS) are frequent in peritoneal dialysis (PD). The Lipoprotein Combine Index (LCI) integrates lipid parameters, but its relationship with peritoneal transport and OS is unclear. Methods: This cross-sectional study included 100 clinically stable adults on continuous ambulatory PD with preserved ultrafiltration and adequate dialysis. LCI was calculated as (total cholesterol × triglycerides × LDL-C)/HDL-C and analyzed by tertiles. Lipid peroxidation and antioxidant markers were measured in serum, erythrocytes, urine, and spent dialysate. Multivariable regression models examined associations between LCI, peritoneal solute transport, and dialysate OS markers. Results: Higher LCI was independently associated with lower peritoneal solute transport. LCI correlated inversely with the 4 h dialysate-to-plasma creatinine ratio (ρ = −0.32, p = 0.001) and remained significant after adjustment (adjusted R² = 0.224, p < 0.001). Increasing LCI was associated with higher malondialdehyde levels in serum, urine, and dialysate (all p ≤ 0.008) and impaired antioxidant defenses, including lower total peroxidase activity in erythrocytes and dialysate (both p = 0.001), reduced serum sulfhydryl groups (p = 0.011), decreased oxidative resistance of erythrocytes, and increased peroxide-induced hemolysis (both p = 0.001). In adjusted models, logLCI was independently associated with higher dialysate malondialdehyde (p < 0.001) and lower dialysate peroxidase activity (p = 0.005). Conclusions: In clinically stable PD patients, higher lipid burden assessed by LCI is independently associated with lower peritoneal solute transport and a marked increase in systemic and local OS. Our findings suggest that dyslipidaemia may contribute to early metabolic and oxidative changes even before overt peritoneal membrane dysfunction develops. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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20 pages, 1982 KB  

Open AccessArticle

A Novel Protective Strategy Against Metformin-Induced Renal Injury Involving Adenosine Triphosphate and Thiamine Pyrophosphate

by Huseyin Kocaturk, Fevzi Bedir, Bulent Yavuzer, Esra Tuba Sezgin, Renad Mammadov, Bahadir Suleyman, Cengiz Sarigul, Ferda Keskin Cimen, Mehmet Sefa Altay and Halis Suleyman

Int. J. Mol. Sci. 2026, 27(4), 1825; https://doi.org/10.3390/ijms27041825 - 14 Feb 2026

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Abstract

Metformin is widely used in type 2 diabetes, but its effects on oxidative and inflammatory pathways remain controversial. Beyond glycemic control, it may promote lactic acidosis by impairing mitochondrial metabolism and pyruvate flux. The potential renoprotective roles of adenosine triphosphate (ATP) and thiamine [...] Read more.

Metformin is widely used in type 2 diabetes, but its effects on oxidative and inflammatory pathways remain controversial. Beyond glycemic control, it may promote lactic acidosis by impairing mitochondrial metabolism and pyruvate flux. The potential renoprotective roles of adenosine triphosphate (ATP) and thiamine pyrophosphate (TPP) remain poorly defined. This study aimed to evaluate whether ATP and TPP mitigate metformin-induced renal injury through biochemical and histopathological assessments. Wistar rats were randomly divided into six groups: control, ATP, TPP, metformin, ATP + metformin, and TPP + metformin. Metformin (50 mg/kg, oral), ATP (4 mg/kg, intraperitoneal), or TPP (20 mg/kg, intraperitoneal) was administered daily for 10 days. Oxidative stress markers, inflammatory cytokines, renal histopathology, and serum creatinine, BUN, lactate, and LDH levels were evaluated. Metformin induced significant oxidative stress, inflammation, metabolic disturbance, and renal injury. ATP provided partial protection, whereas TPP markedly restored redox balance, reduced inflammation, and preserved renal histology. TPP confers superior protection against metformin-induced renal injury compared with ATP by modulating oxidative, inflammatory, and metabolic pathways, highlighting its therapeutic potential in preventing metformin-related nephrotoxicity. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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21 pages, 7325 KB  

Open AccessArticle

Choline Deficiency Drives the Inflammation–Fibrosis Cascade: A Spatiotemporal Atlas of Hepatic Injury from Weeks 6 to 10

by Shang Li, Guoqiang Zhang, Xiaohong Li, Xu Zhao, Axi Shi, Qingmin Dong, Changpeng Chai, Xiaojing Song, Yuhui Wei and Xun Li

Antioxidants 2026, 15(1), 110; https://doi.org/10.3390/antiox15010110 - 15 Jan 2026

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Abstract

Metabolic dysfunction-associated steatotic liver disease (MASLD) is strongly linked to systemic metabolic disturbances and features a lipid-driven cascade that promotes hepatic inflammation and fibrosis. Choline insufficiency contributes to disease advancement by altering phospholipid turnover and redox homeostasis; however, its spatial and temporal regulatory [...] Read more.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is strongly linked to systemic metabolic disturbances and features a lipid-driven cascade that promotes hepatic inflammation and fibrosis. Choline insufficiency contributes to disease advancement by altering phospholipid turnover and redox homeostasis; however, its spatial and temporal regulatory roles throughout MASLD progression remain insufficiently defined. A 10-week high-fat, choline-deficient (HFCD) mouse model was established, and liver pathology was evaluated at weeks 6, 8, and 10. Time-resolved assessments combined untargeted metabolomics, magnetic resonance imaging–proton density fat fraction (MRI-PDFF), serum biochemistry, histological staining, immunofluorescence, and transmission electron microscopy to characterize dynamic alterations in lipid metabolism, redox status, inflammation, and fibrogenesis. The HFCD diet produced a clear temporal sequence of liver injury. Steatosis, phosphatidylcholine depletion, and early antioxidant loss appeared by week 6. By week 8, mitochondrial structural damage and pronounced cytokine elevation were evident. At week 10, collagen deposition and α-SMA activation signaled fibrotic progression. Metabolomics indicated significant disruptions in pathways related to ATP-binding cassette (ABC) transporters, one-carbon metabolism, and the tricarboxylic acid (TCA) cycle. Using integrated analytical strategies, this study suggests that choline deficiency may be associated with a time-dependent pathological cascade in MASLD, beginning with phospholipid destabilization and extending to altered mitochondria–endoplasmic reticulum crosstalk at mitochondria-associated membranes, alongside amplified oxidative–inflammatory responses, which collectively may contribute to progressive fibrogenesis as the disease advances. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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14 pages, 1469 KB  

Open AccessArticle

Mitigating Hydroxychloroquine-Induced Oxidative Liver Damage: The Roles of Adenosine Triphosphate, Liv-52, and Their Combination in Rats

by Meryem Yalvac Kandefer, Esra Tuba Sezgin, Bahadir Suleyman, Ferda Keskin Cimen, Fulya Memiş, Mine Gulaboglu and Halis Suleyman

Int. J. Mol. Sci. 2026, 27(1), 421; https://doi.org/10.3390/ijms27010421 - 31 Dec 2025

Viewed by 700

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Hydroxychloroquine (HCQ), originally developed as an antimalarial agent, has been associated with hepatotoxic effects in experimental and clinical settings. Our study was designed to evaluate the effects of this agent on liver toxicity and to understand the protective roles of adenosine triphosphate (ATP), [...] Read more.

Hydroxychloroquine (HCQ), originally developed as an antimalarial agent, has been associated with hepatotoxic effects in experimental and clinical settings. Our study was designed to evaluate the effects of this agent on liver toxicity and to understand the protective roles of adenosine triphosphate (ATP), Liver-52 (Liv-52), and their combination. Male Wistar rats (250–280 g) were randomly assigned to five groups (n = 6): healthy control (C), HCQ only (H), ATP plus HCQ (AH), Liv-52 plus HCQ (LH), and ATP–Liv-52 plus HCQ (ALH). ATP (4 mg/kg) was administered intraperitoneally once daily, whereas Liv-52 (20 mg/kg) was administered orally via gavage. One hour later, all groups except C received HCQ (120 mg/kg, orally, twice daily). All treatments were continued for seven consecutive days. At the end of the experiment, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured, and liver tissues were analyzed for malondialdehyde (MDA), total glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities, along with histopathological evaluation. HCQ administration significantly increased oxidative stress, as evidenced by elevated MDA levels (p < 0.01) and reduced antioxidant parameters, including GSH, SOD, and CAT (p < 0.05), accompanied by prominent histopathological damage. Treatment with ATP or Liv-52 markedly ameliorated these alterations by decreasing MDA and restoring antioxidant markers. The combination treatment was observed to exhibit the most pronounced protective effect; it significantly reduced MDA levels, improved GSH, SOD, and CAT levels more effectively, and produced significant decreases in AST and ALT values (p < 0.05). Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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Open AccessReview

Role of Matricellular Proteins in Endothelial Cell Inflammation and Atherosclerosis

by Ravi Varma Aithabathula, Santosh Kumar and Bhupesh Singla

Antioxidants 2025, 14(11), 1338; https://doi.org/10.3390/antiox14111338 - 6 Nov 2025

Cited by 1 | Viewed by 2000

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The vascular endothelium serves as a critical barrier preventing the transmigration of monocytes, circulating lipoproteins, and other molecules into the subendothelial space, and plays a vital role in regulating vascular tone. A dysfunctional and inflamed endothelial layer in response to disturbed blood flow [...] Read more.

The vascular endothelium serves as a critical barrier preventing the transmigration of monocytes, circulating lipoproteins, and other molecules into the subendothelial space, and plays a vital role in regulating vascular tone. A dysfunctional and inflamed endothelial layer in response to disturbed blood flow or other proatherogenic risk factors is the initiating event in the pathogenesis of atherosclerosis, suggesting the importance of an intact and properly functioning endothelium in preventing the onset and progression of this disease. Accumulated evidence demonstrates the significant role of matricellular proteins, which are non-structural and secretory extracellular matrix (ECM) proteins, in the development of atherosclerosis. These proteins exert multifaceted effects on endothelial cells (ECs) ranging from reactive oxygen species (ROS) production, endoplasmic reticulum stress, and expression of adhesion molecules to autophagy and compromised barrier function via stimulating various molecular mechanisms. Given the critical roles of these processes in EC function and atherosclerosis, a better understanding of signaling pathways governed by matricellular proteins in ECs is required to develop therapeutic strategies for suppressing or preventing atherosclerosis and related cardiovascular diseases (CVDs). This review comprehensively summarizes the existing literature on the diverse roles of matricellular proteins in regulating EC inflammation and function, and highlights their potential as viable therapeutic targets for maintaining vascular health and inhibiting the progression of atherosclerosis. Full article

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17 pages, 1319 KB  

Open AccessArticle

Oxidative Stress Score as an Indicator of Pathophysiological Mechanisms Underlying Cardiovascular Disease in Kidney Transplant Recipients

by Valera-Arévalo Gemma, Paula Jara Caro, María del Mar Rodríguez-San Pedro, Claudia Yuste, María Gabriela Ortiz-Diaz, Rafael Ramírez, Matilde Alique, Natalia Guerra-Pérez, Julia Carracedo and Enrique Morales

Oxygen 2025, 5(4), 20; https://doi.org/10.3390/oxygen5040020 - 16 Oct 2025

Cited by 1 | Viewed by 1444

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Chronic kidney disease is closely associated with an increased risk of cardiovascular disease. Although kidney transplantation represents the treatment of choice for patients with end-stage chronic kidney disease, it is also linked to significant cardiovascular risk. This study aimed to evaluate the relationship [...] Read more.

Chronic kidney disease is closely associated with an increased risk of cardiovascular disease. Although kidney transplantation represents the treatment of choice for patients with end-stage chronic kidney disease, it is also linked to significant cardiovascular risk. This study aimed to evaluate the relationship between cardiovascular pathology and oxidative status in kidney transplant recipients, while also assessing the influence of disease etiology and humoral immune response on oxidative imbalance. A cross-sectional analysis was conducted in individuals with advanced chronic kidney disease (n = 36) and kidney transplant recipients (n = 40). A total of 18 healthy subjects were included. The enzymatic activities of xanthine oxidase, superoxide dismutase, and glutathione peroxidase, and levels of lipid peroxidation products, oxidized glutathione, and reduced glutathione were measured using spectrophotometry in plasma and mononuclear and polymorphonuclear leukocytes isolated using Ficoll density gradients. Individual oxidative status was evaluated using OXYSCORE. Kidney transplantation was associated with a higher incidence of cardiovascular disease (p < 0.01) and increased levels of both prooxidant (p < 0.01) and antioxidant parameters (p < 0.01). Elevated OXYSCORE values were observed particularly in patients with nephroangiosclerosis, diabetic kidney disease, polycystic kidney disease (p < 0.05), and cardiovascular comorbidities (p < 0.001). Additionally, the presence of anti-graft antibodies correlated with higher oxidative scores. These findings suggest that OXYSCORE may serve as a potential indicator of cardiovascular damage in kidney transplant recipients. Full article

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11 pages, 3848 KB  

Open AccessArticle

Preventive and Therapeutic Effects of Hydrogen-Generating Si-Based Agent on Pressure Ulcers in Mice

by Naoya Otani, Takaki Oue, Yuki Kobayashi, Hikaru Kobayashi, Koichi Tomita and Tateki Kubo

Biomedicines 2025, 13(10), 2475; https://doi.org/10.3390/biomedicines13102475 - 11 Oct 2025

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Objectives: As a known antioxidant, hydrogen has been useful for treating pressure ulcers. However, conventional methods of hydrogen administration have limitations with regard to dosage and continuity of hydrogen intake. This study evaluated the efficacy of a novel Si-containing agent that can [...] Read more.

Objectives: As a known antioxidant, hydrogen has been useful for treating pressure ulcers. However, conventional methods of hydrogen administration have limitations with regard to dosage and continuity of hydrogen intake. This study evaluated the efficacy of a novel Si-containing agent that can generate substantial quantities of hydrogen to treat pressure ulcers in an in vivo mouse model. Methods: The back skin and subcutaneous tissue of mice were compressed with magnets for 12 h. Changes in the ulcer area after release of compression, histological findings, degree of apoptosis, and expression levels for oxidative stress markers and inflammation-related cytokines were compared between mice fed a normal diet (control group) and those fed a 2.5 wt% Si-based diet (Si group). Results: The Si group had a significantly smaller ulcer area and shorter healing period than the control group. Moreover, inflammatory responses, apoptotic activity, and oxidative stress within the ulcer tissue were suppressed significantly in the Si group. Conclusions: Oral intake of the Si-based agent can potentially treat and prevent pressure ulcers by regulating apoptosis, oxidative stress, and inflammatory responses. Full article

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16 pages, 4051 KB  

Open AccessArticle

Protective Effect of Exogenous Adenosine Triphosphate Against Ocular Toxicity of Linezolid in Rats

by Cenap Mahmut Esenulku, Ibrahim Cicek, Ahmet Mehmet Somuncu, Bulent Yavuzer, Esra Tuba Sezgin, Tugba Bal Tastan, Nurinisa Yücel, Ezgi Karatas and Halis Suleyman

Life 2025, 15(10), 1587; https://doi.org/10.3390/life15101587 - 11 Oct 2025

Cited by 1 | Viewed by 782

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Linezolid, a synthetic antimicrobial agent, may induce oxidative damage in ocular tissues, particularly in the optic nerve. Adenosine triphosphate (ATP) is involved in the production of antioxidants that scavenge and neutralize reactive oxygen species. This study aims to evaluate the potential protective effect [...] Read more.

Linezolid, a synthetic antimicrobial agent, may induce oxidative damage in ocular tissues, particularly in the optic nerve. Adenosine triphosphate (ATP) is involved in the production of antioxidants that scavenge and neutralize reactive oxygen species. This study aims to evaluate the potential protective effect of exogenous ATP against linezolid-induced ocular damage in rats, in comparison with methylprednisolone. Wistar-type rats were divided into five groups as follows: healthy (HG), ATP-only (ATPG), linezolid-only (LZDG), ATP + linezolid (ATLDG), and methylprednisolone + linezolid groups (MPLDG). Oxidative stress markers, antioxidant biomarkers, and proinflammatory cytokines were analyzed in isolated ocular tissues. Optic nerve tissue was also evaluated histopathologically. Linezolid administration increased the oxidative stress marker MDA and the proinflammatory cytokine TNF-α, while decreasing antioxidant parameters such as tGSH, SOD and CAT in rat ocular tissues, compared to the healthy group. However, it did not significantly alter serum troponin I levels. Histopathological analysis revealed that linezolid induced oxidative damage and inflammation in optic nerve tissue, with marked glial alterations. ATP administration reduced linezolid-induced oxidative stress in ocular tissue, as indicated by decreased MDA levels. It also enhanced antioxidant defenses by increasing tGSH, SOD, and CAT levels. In addition, ATP lowered proinflammatory cytokine levels, thereby alleviating inflammation. These effects collectively contributed to the restoration of biochemical parameters toward normal levels. In addition, ATP mitigated linezolid-induced optic nerve damage and glial alterations. The critical role of ATP in reducing oxidative stress, restoring antioxidant balance, and suppressing inflammation may represent a promising therapeutic approach for linezolid-induced ocular toxicity. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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18 pages, 3287 KB  

Open AccessArticle

In Silico and In Vitro Studies of Anti-Inflammatory, Anti-Oxidative Stress, and Anti-Apoptosis Effect of 7-Octenoic Acid Derived from Moringa oleifera Lam., on LPS-Induced Monocyte-Derived Macrophages (MDM)

by Kittipong Srimuang, Watunyoo Buakaew, Yordhathai Thongsri, Krai Daowtak, Pachuen Potup, Antonio Ferrante and Kanchana Usuwanthim

Int. J. Mol. Sci. 2025, 26(18), 8911; https://doi.org/10.3390/ijms26188911 - 12 Sep 2025

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Abstract

While Moringa oleifera Lam. (MO) extracts are known to have various bioactive properties, including anti-inflammatory properties, the components responsible still remain to be identified. This study explores the protective effects of the MO component, 7-octenoic acid (7OCT) in LPS-stimulated THP-1 macrophage inflammatory responses. [...] Read more.

While Moringa oleifera Lam. (MO) extracts are known to have various bioactive properties, including anti-inflammatory properties, the components responsible still remain to be identified. This study explores the protective effects of the MO component, 7-octenoic acid (7OCT) in LPS-stimulated THP-1 macrophage inflammatory responses. The compound significantly downregulated the production of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6, as well as the expression of inflammation-related genes NFKB1, PTGS2, and NOS2. Additionally, it inhibited the nuclear translocation of NF-κB p65, a key transcription factor of inflammatory signaling cascade. Effects on oxidative stress showed that 7OCT inhibited LPS-induced NADPH oxidase 2 (NOX2) component genes including CYBB, CYBA, NCF1, NCF2, and NFE2L2, along with phosphorylated NOX2 and p47^phox proteins. The compound reduced the expression of TP53, BAX, CASP3, and CASP7, while enhancing BCL2 expression and Bcl-2 protein levels, suggesting an effect on apoptosis. Decreased levels of BAX, caspase-3, and cleaved caspase-3 proteins further confirmed its anti-apoptotic effect. Our findings suggest that 7OCT exhibits strong anti-inflammatory, antioxidant, and anti-apoptotic properties. Full article

(This article belongs to the Topic Oxidative Stress and Inflammation, 3rd Edition)

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