Search Results (4,644)

Objective: In this study, Dehydroepiandrosterone (DHEA-induced Polycystic Ovary Syndrome (PCOS) mice were used as models to evaluate the improvement effect of Vitexin (Vit) on ovarian fibrosis and explore the mechanism of action of the NR4A1/NLRP3 signaling pathway. Method: Sixty 4-week-old female ICR mice of the same batch number were selected and their systems were divided into 6 groups (n = 10): normal (Control, Ctrl) group, model (Polycystic Ovary Syndrome, PCOS) group, treatment (Vitexin, The Vit group, normal NR4A1 gene silencing group (Ctrl NR4A1^-/-), NR4A1 gene silencing model group (PCOS NR4A1^-/-), and NR4A1 gene silencing treatment group (Vit NR4A1^-/-). Silencing gene modeling was performed by tail vein injection of adeno-associated virus (serotype AAV-8), and the mouse genotypes were detected by qRT-PCR technology 14 days after injection. After the genotype was determined, the PCOS group and the PCOS NR4A1^-/- group were administered dehydroepandrosterone (6 mg/100 g/d) by gavage for 28 consecutive days for modeling, while the Vit group and the Vit NR4A1^-/- group were treated with dehydroepandrosterone + vitexin (10 mg/kg/d) by gavage for 28 consecutive days. All mice were raised with pure water and regular maintenance food. After 4 weeks of drug intervention, the mice were euthanized and samples were collected. The pathological changes in ovarian tissue were observed by H&E staining, and the degree of ovarian tissue fibrosis was observed by Masson staining. The levels of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), total cholesterol (TC), triglycerides (TG), high-density lipoprotein cholesterol (HDL-C), and low-density lipoprotein cholesterol (LDL-C) in mouse serum were detected by biochemical kits. The levels of inflammatory factors (IL-1β, IL-6, IL-18, TNF-α) in mouse serum were determined by enzyme-linked immunosorbent assay. Real-time fluorescence quantitative PCR (qRT-PCR) was used to detect oxidative kinase (Gsta4, Prdx3, Mgst1, Gpx3, Gsr), inflammatory factors (Nlrp3, Caspase-1, Asc, Il-1β, Il-18, Tnf-α) and fibrotic pathway-related genes (Tgf-β1, Smad3, Collagen1, CTGF, α-SMA, Mmp-13, and β-catenin) in ovarian tissues. The levels of inflammatory factors (NLRP3, Caspase-1, ASC, IL-1β, IL-18, TNF-α, IκBα) and fibrosis in mice were determined by Western blot method, and statistical description and analysis were performed using SPSS software. Result: In the wild-type genotype group, compared with the PCOS group, Vit treatment could effectively regulate the metabolic abnormalities of PCOS mice, including inhibiting excessive weight gain, restoring normal glucose tolerance, and reducing body fat content. After Vit treatment, the levels of MDA, TC, TG, LDL, IL-1β, IL-6, IL-18 and TNF-α in the serum of PCOS mice were significantly reduced, while the levels of SOD and HDL in the serum of PCOS mice were increased. The staining results indicated that Vit treatment could significantly inhibit the process of ovarian fibrosis in PCOS mice. The results of WB and PCR demonstrated that after Vit gavage treatment in mice, inflammatory and fibrotic factors such as Nlrp3, Caspase-1, Asc, Il-1β, Il-18, Tgf-β1, Smad3, Collagen1, CTGF, and α-SMA in ovarian tissues could be significantly down-regulated, and the fibrotic level of ovarian tissues could be reduced. Among the same measurement indicators, the silenced NR4A1 group showed a certain degree of increase compared with the wild genotype group, but there was no significant difference. Conclusions: Vit intervention can restore the sex hormone levels and follicular development in ovarian tissues of PCOS mice, regulate reproductive endocrine disorders and abnormal lipid metabolism levels, and regulate the expression of Collagen I, a-SMA and CTGF in the ovaries by inhibiting the NR4A1/NLRP3 signaling pathway, thereby improving the ovarian fibrosis level of PCOS mice. It is suggested that it may play a key role in the treatment of PCOS and the prevention and delay of its long-term complications. Full article

Methylglyoxal (MG) is a reactive dicarbonyl compound generated mainly as a byproduct of glycolysis. Excess accumulation of MG can promote protein glycation and the formation of advanced glycation end-products (AGEs), which have been associated with oxidative stress, inflammation, mitochondrial dysfunction, and cellular damage. These processes are implicated in the development of several chronic conditions, including diabetes, neurodegenerative disorders, cardiovascular disease, and age-related decline. The glyoxalase system, comprising Glyoxalase I (Glo1) and Glyoxalase II (Glo2), serves as a key cellular defense mechanism that detoxifies MG and helps maintain dicarbonyl homeostasis. Among these enzymes, Glo1 catalyzes the conversion of MG into less reactive intermediates in a glutathione (GSH)-dependent manner. A range of natural compounds and dietary phytochemicals, including sulforaphane, resveratrol, α-lipoic acid, selenium, vitamin D3, and N-acetylcysteine, have been reported to modulate Glo1 activity through transcriptional regulation, antioxidant effects, or support of intracellular GSH levels. Evidence from preclinical and limited human studies suggests that these compounds may help reduce MG burden and AGE formation, although their effects are often indirect and context-dependent. However, several challenges remain, including variable bioavailability, dose-dependent responses, disease-specific differences in Glo1 regulation, and the lack of standardized biomarkers and adequate clinical validation. This review examines the MG–Glo1 axis as a mechanistic framework linking metabolic stress to disease and evaluates natural compounds as context-dependent modulators of this pathway. By integrating mechanistic insights with emerging in vivo and clinical evidence, this work highlights the potential, while acknowledging the limitations, of targeting Glo1 as a translational strategy for managing glycation-associated disorders. Full article

Cardiac surgery-associated acute kidney injury (CSA-AKI) is a frequent and severe complication of open-heart surgery. Although oxidative/inflammatory mechanisms are known to contribute to its pathophysiology, the circulating factors involved are poorly understood. In this preliminary investigation, we evaluated the effects of plasma from patients undergoing cardiac surgery on endothelial and renal tubular cells at anesthesia induction (T0) and 48 h after surgery (T1). Plasma levels of thiobarbituric acid-reactive substances (TBARSs), glutathione (GSH), and nitric oxide (NO) were measured in parallel. At T0, patient plasma showed increased TBARSs and reduced GSH and NO levels, consistent with oxidative imbalance, and induced cellular injury. In both cell types, plasma exposure reduced cell viability and mitochondrial membrane potential, while it increased oxidant release. Endothelial cells also showed decreased NO production, whereas renal tubular displayed increased apoptotic markers and reduced anti-aging factors. At T1, these alterations were further aggravated only in patients who developed CSA-AKI, whose plasma caused more severe endothelial and tubular damage. These findings support the presence of circulating injurious factors in cardiac surgery patient plasma that may contribute to CSA-AKI pathogenesis and help identify patients at risk before irreversible kidney damage develops. Full article

Weanling piglets, with immature immune system and physiological functions, often experience post-weaning diarrhea. This study investigated the effects of combined supplementation of live yeast and yeast postbiotics on the growth performance, antioxidant capacity and intestinal health of weaned piglets. A total of 224 weaned piglets (22 days old) were randomly assigned to four groups: a basal diet (CON) or the same diet supplemented with 1600 ppm zinc oxide (ZnO), high-dose live yeast and yeast postbiotics (LYYP-H), or low-dose live yeast and yeast postbiotics (LYYP-L). The trial lasted 28 days, with diets divided into 2 phases. The results showed that dietary combined supplementation with live yeast and yeast postbiotics did not significantly affect the average daily gain (ADG), average daily feed intake (ADFI), or the diarrhea rate (p > 0.05). However, dietary combined supplementation with live yeast and yeast postbiotics significantly enhanced fecal consistency in piglets (p < 0.05). Moreover, dietary combined supplementation with live yeast and yeast postbiotics significantly improved representative antioxidant indices, notably superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and strengthened immune capabilities; additionally, a marked improvement in intestinal morphology was observed (p < 0.05). In conclusion, the combination of live yeast and yeast postbiotics can improve antioxidant capacity and intestinal health and show the potential to replace high doses of ZnO during the first two weeks post-weaning. Full article

Background: This pilot study examined whether oxidative–nitrosative stress is associated with clinical status in amyotrophic lateral sclerosis (ALS). We analyzed associations between plasma markers of oxidative–nitrosative imbalance and ALSFRS–R, disease duration, survival, and routine biochemical parameters. Methods: Twenty-nine ALS patients fulfilling the Gold Coast diagnostic criteria were enrolled. Plasma levels of 3-nitrotyrosine (3–NT), 8-oxo-2′-deoxyguanosine (8–oxodG), malondialdehyde (MDA), glutathione (GSH), non-protein thiols (NP–SH), and non-protein disulfides (NP–SS–NP), as well as creatinine, urea, uric acid and BMI, were measured. Associations with ALSFRS–R and disease duration were evaluated using non-parametric correlation analyses and second-order polynomial regression (adjusted R²), while survival was explored using Kaplan–Meier analysis and multivariable Cox regression. Given the modest sample, we considered statistical power and applied Benjamini–Hochberg false discovery rate (FDR) correction within marker families. Results: At the uncorrected significance level, 3–NT showed a positive correlation with ALSFRS–R and a negative correlation with disease duration, and NP–SH correlated negatively with disease duration; however, these associations did not remain significant after FDR correction (FDR-adjusted p ≥ 0.099). Other oxidative–nitrosative markers and biochemical parameters showed no robust relationships with clinical measures. In Cox models, 3–NT was not significantly associated with survival (HR 3.44 per 1 nM, 95% CI 0.25–47.97, p = 0.358), whereas older age predicted higher mortality (HR 1.05 per year, 95% CI 1.00–1.10, p = 0.036). Conclusions: 3–NT and NP–SH exhibited the strongest trends among the investigated markers, but their clinical associations in this small cross-sectional cohort remain exploratory and require confirmation in larger longitudinal studies. Full article

Background/Objectives: Inflammation and oxidative stress are key factors contributing to the initiation and progression of liver fibrosis in chronic obstructive cholestasis. Pantothenic acid (PA) and some of its derivatives have been reported to exhibit moderate anti-inflammatory, antioxidant, and regenerative effects. This study aimed to evaluate the redox-modulating effects of PA derivatives—panthenol (PL), pantethine (PT), and hopantenic acid (HPA) in a rat model of chronic obstructive cholestasis induced by common bile duct ligation (BDL). Methods: Macroscopic, histological, and ultrastructural alterations in the liver were assessed, along with molecular markers of oxidative stress, inflammation, and parameters of the glutathione (GSH) system. Results: BDL-induced liver injury was associated with enhanced lipid peroxidation, mitochondrial structural alterations, depletion of GSH, increased levels of protein S-glutathionylation (PSSG), and elevated thiobarbituric acid-reactive substances in mitochondria. Treatment with PL and, to a lesser extent, PT was associated with attenuation of hepatocellular ultrastructural damage, reduced bile duct hyperplasia, decreased inflammatory and necrotic changes, and moderate improvement in fibrosis-related parameters. In contrast, HPA (a PA antagonist) did not demonstrate hepatoprotective effects and it was associated with more pronounced liver injury. Conclusions: Chronic BDL is accompanied by suppression of glutathione redox capacity and enhanced oxidative stress. PL and PT, but not HPA, were associated with reduced levels of protein S-glutathionylation and partial restoration of redox balance. The protective effects of PL and PT may contribute to their antifibrotic activity, potentially through direct antioxidant capacity or redox-modulating mechanisms associated with the GSH system. Full article

Licorice is a traditional Chinese medicine; however, its bioactive constituents and specific molecular mechanisms responsible for protecting against radiation-induced brain injury remain poorly elucidated. Oxidative stress overactivation acts as the core pathological mechanism underlying radiation-triggered neuronal injury. This study aimed to investigate the neuroprotective effect and underlying mechanism of isoliquiritigenin (ISL), a major blood-absorbed component of licorice, against radiation-induced neural injury in C57BL/6J mice via the Keap1-Nrf2 signaling pathway. Molecular docking and MST analysis verified the strong binding affinity of ISL to Keap1. In vitro, ISL restored the viability of X-ray-irradiated PC12 cells; reduced LDH release and intracellular ROS accumulation; and enhanced SOD1 activity, GSH content, and T-AOC levels. Moreover, ISL upregulated the expression of antioxidant-related genes and induced Nrf2 nuclear translocation. In vivo, oral ISL administration ameliorated radiation-induced cognitive impairment, improved spatial learning and memory, alleviated hippocampal neuronal loss, and increased cerebral cortical Nrf2 expression in C57BL/6J mice. In conclusion, ISL alleviates radiation-induced neuronal injury by suppressing oxidative stress and activating the Keap1-Nrf2 signaling pathway, thus representing a promising therapeutic agent for the prevention and treatment of radiation brain injury. Full article

Natural products remain a major source of anticancer agents, yet freshwater organisms are largely unexplored. Building on our previous evidence that planarian mucus exerts cytostatic and cytotoxic effects on cancer cells, we investigated the involvement of endoplasmic reticulum stress and unfolded protein response (UPR) pathways. Mucus-induced cytotoxicity is ROS-dependent and associated with depletion of intracellular reduced glutathione (GSH), not through inhibition of the System Xc⁻ transporter but potentially associated with upregulation of CHAC1, a glutathione-degrading enzyme. Mucus fractionation based on molecular weight identified the high-molecular-weight crude fraction as the one containing the bioactive entity, reproducing the effects of whole mucus. Treatment with this fraction early activates the PERK–ATF4 branch of the UPR, which could be responsible for driving CHAC1 induction. Moreover, ATF4 enhances DDIT3 expression, and activates a compensatory NRF2-dependent antioxidant response. At a later stage mucus also activates the IRE1α–XBP1 axis, with no ATF6 involvement, indicating selective UPR engagement in response to oxidative and lipid stress. Overall, our data are consistent with a potential PERK–ATF4–CHAC1–GSH self-sustaining axis promoting oxidative stress that culminates in cell death, supporting the potential of planarian mucus as a source of pleiotropic bioactive compounds, although the molecular identity of the active component(s) remains still unresolved. Full article

Heat stress (HS) has emerged as a major environmental stressor, inducing oxidative stress and hepatic steatosis and impairing production performance and health in laying hens, with limited evidence-based nutritional interventions available. This study investigated the hepatoprotective effects of dietary silibinin (SIL) against chronic HS. In a 10-week trial, 252 43-week-old Hy-Line Brown hens were exposed to daily HS (32 ± 1 °C, temperature–humidity index [THI] > 73) and fed either a basal diet or one supplemented with 100 mg/kg SIL. SIL significantly increased laying rate (p < 0.05) and improved albumen height, Haugh units, and shell strength by week 8 (p < 0.05). Histological analysis showed a 48% reduction in non-alcoholic fatty liver disease (NAFLD) activity score, with significantly decreased hepatic triglyceride content (p < 0.05); Oil Red O staining confirmed reduced lipid droplet accumulation. SIL restored redox balance by increasing plasma, hepatic total superoxide dismutase (T-SOD), and glutathione peroxidase (GSH-Px) (p < 0.05), increasing hepatic catalase (CAT) and glutathione (GSH) levels while decreasing malondialdehyde (MDA) (p < 0.05). Untargeted plasma metabolomics identified 11 key metabolites related to 2-oxoglutarate and purine metabolism, while hepatic transcriptomics revealed 835 differentially expressed genes primarily in the PPAR signaling and fatty acid biosynthesis pathways. SIL suppressed de novo lipogenesis via downregulation of ACACA and FASN, and enhanced β-oxidation through upregulation of CPT1A and ACSL1 (p < 0.05). Molecular docking indicated favorable binding affinities between SIL and these targets, which was further supported by corresponding changes in protein expression via Western blotting. Correlation analysis revealed a consistent alignment between the upregulation of ACSL1/CPT1A and improvement in performance and antioxidant status, suggesting a coordinated metabolic shift. These findings emphasize the potential of SIL as a sustainable animal nutrition antioxidant additive, which can alleviate HS-induced lipid disorders in the liver of laying hens. Importantly, these hepatoprotective effects were demonstrated exclusively under chronic heat stress conditions; further studies incorporating a normothermic baseline are required to distinguish stress-specific mitigation from general metabolic stimulation. Full article

Diabetic kidney disease (DKD) is a primary cause of end-stage renal disease (ESRD), and while ferroptosis is known to contribute to DKD pathogenesis, the regulatory role of the NLRP3 inflammasome in this process remains elusive. To address this research gap, we explored whether NLRP3 inhibition alleviates DKD by suppressing ferroptosis using streptozotocin-induced diabetic wild-type and NLRP3-knockout C57BL/6 mice, alongside high-glucose-cultured (30 mM) human renal tubular epithelial (HK-2) cells with or without siNLRP3 transfection. Inflammatory cytokines (IL-6, TNF-α, and IL-1β) were measured using an ELISA; oxidative stress markers (CSSG, MDA, GSH, and ROS) and the iron ion content via colorimetric assays; mitochondrial morphology by transmission electron microscopy (TEM); and ferroptosis-related proteins (ACSL4, COX2, and GPX4) through Western blotting. Our findings demonstrate that NLRP3-knockout diabetic mice displayed markedly reduced urinary albumin excretion and serum creatinine levels (p < 0.01) compared with wild-type diabetic controls, concurrent with suppressed renal iron overload and ferroptosis, diminished inflammatory cytokine levels, and attenuated oxidative stress. Pathological assessments further revealed ameliorated renal fibrosis and preserved mitochondrial ultrastructure in NLRP3-deficient mice. In vitro, siNLRP3 transfection abrogated high-glucose-induced inflammation, oxidative stress, and ferroptosis in HK-2 cells, effects that were reversed by the ferroptosis inducer erastin (p < 0.01). Mechanistically, NLRP3 deficiency was associated with upregulated GPX4 expression and downregulated ACSL4 and COX2 expression. Collectively, these results indicate that inhibition of the NLRP3 inflammasome mitigates DKD progression by suppressing ferroptosis, underscoring its translational potential as a therapeutic target for this condition. Full article

The liver is a critical organ in drug metabolism and detoxification. Ganoderma lingzhi triterpenoids, a major class of bioactive compounds in G. lingzhi extracts, exhibit liver protective effects with pharmaceutical potential. In this study, we established an acute liver injury model in mice via intraperitoneal injection of 0.25% Carbon tetrachloride(CCl₄) olive oil. Prophylactic and therapeutic administration of G. lingzhi triterpenoid extracts were evaluated using alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and hepatic histopathology. Western blot analysis assessed protein expression of anti-inflammatory and antioxidant stress-related pathways (Nrf2/Keap1 and MyD88/NF-κB-p65). Intervention effects on acute liver injury were determined by measuring protein molecular weight following triterpenoid treatment. In summary, G. lingzhi triterpenoids significantly alleviate oxidative stress and inflammatory responses in mice with acute liver injury by activating the KEAP1-Nrf2 antioxidant pathway and inhibiting the NF-κB-p65 and MyD88-mediated inflammatory pathways. These triterpenoids reduced serum transaminase levels, improved hepatic histopathological damage, and exerted effective protective effect on liver tissue. This study provides experimental support for the comprehensive evaluation of G. lingzhi’s anti-inflammatory and antioxidant effects. Full article

Panax vietnamensis var. fuscidiscus, or PVF, a member of Araliaceae, is a new and high-value variety of Vietnamese Ginseng (P. vietnamensis var. vietnamensis—VG). PVF shares some similarities in terms of its saponin profile with VG, including protopanaxadiol, protopanaxatriol, and ocotillol saponin. Previous research has revealed that the steaming process significantly increases the bioactivities of VG, especially the renal protective effect. In this study, PVF roots were steamed at a high temperature (120 °C) for 12 h to obtain Black PVF (BPVF). The BPVF extract was tested in both in vitro and in vivo models of cisplatin toxicity to assess its antioxidant and nephroprotective activities. The results showed that the BPVF obtained from the steaming process exhibited the highest antioxidant activity at 12 h. The chemical composition of BPVF is characterized by less-polar saponins such as G-Rg3, -Rg5, and ocotillol genin. The BPVF extract (200 mg/kg) reversed kidney injuries by significantly lowering serum creatinine and blood urea nitrogen (BUN) levels, which had increased due to cisplatin toxicity. The antioxidant effect of BPVF extract also prevented lipid peroxidation by lowering malondialdehyde (MDA) levels and restoring redox balance by increasing glutathione (GSH) content in kidney cells to nearly normal levels, with effects comparable to quercetin. This study provides evidence of BPVF’s therapeutic potential with respect to kidney injuries due to cisplatin toxicity. Full article

Copper is a common pollutant in aquatic environments. Excess copper in water can enter aquatic organisms through respiration, feeding, and adsorption, thereby exerting serious adverse effects on their health. In this study, NEW Genetically Improved Farmed (GIFT) Nile tilapia (Oreochromis niloticus L.) was used to explore the effect of copper on the hepatopancreas and post-exposure recovery. Acute exposure was simulated via an intraperitoneal injection of 3.75 mg Cu²⁺/kg body mass, while physiological saline injections served as the control. Samples were collected on days 1, 7, 14, and 21 post-exposure to evaluate growth performance, histopathological changes, antioxidant enzyme activities, and the expression of oxidative stress-related genes in the hepatopancreas. The results show that body length and mass increased within 21 days of the injection and copper exposure did not significantly affect fish growth. On day 1 after copper injection, numerous vacuoles appeared in hepatopancreatic tissues. On day 14, congestion and obvious hepatic sinusoids were observed. However, on day 21, the tissue structure showed gradually recovery. Compared to the control group, superoxide dismutase (SOD) activity was significantly higher in the exposed group on days 1, 14, and 21, and SOD gene expression was significantly elevated on day 21. Catalase (CAT) activity was significantly higher on day 7, and the expression of the CAT gene increased significantly on days 1 and 21. Glutathione peroxidase (GSH-Px) activity decreased significantly on day 7, whereas GPX gene expression increased significantly at the same time point. No significant difference in acetylcholinesterase (AChE) activity was observed during the experiment. In conclusion, copper administered via intraperitoneal injections induced significant activation of the antioxidant defense system and histopathological damage in the hepatopancreas of tilapia. Although tissue damage gradually recovered over time, the activation of the antioxidant defense system partially persisted. Ultimately, copper exposure did not significantly affect growth indicators such as body length and mass. These results advance our understanding of copper toxicity in farmed fish and provide a scientific reference for safe aquaculture production. Full article

Sustainable piglet farming faces challenges from weaning stress, which necessitates the exploration of effective, natural antimicrobial alternatives to enhance growth and gut health. So, this study evaluated the effects of algal oligosaccharide (OSA) supplementation (0, 200, 400, 600, 800 mg/kg) as a natural antimicrobial alternative. Results showed that OSA significantly (p < 0.05) improved slaughter performance and the apparent digestibility of nutrients (OM, CP, amino acids) and energy. OSA increasing serum glucose while decreasing urea nitrogen and cholesterol, suggesting a shift in energy substrate mobilization. Enhanced antioxidant capacity was evidenced by increased T-SOD and GSH-Px activities and reduced MDA content. Immunologically, OSA elevated serum IgA, IgM, and IL-10, while inhibiting pro-inflammatory cytokines (IL-1β, IL-6). In the jejunum, OSA obviously increased disaccharidase activities and sIgA levels. Microbial analysis revealed that OSA favorably modulated cecal microbiota by increasing the abundance of Firmicutes and beneficial genera while decreasing Proteobacteria and potential pathogens (e.g., Escherichia). In conclusion, dietary OSA improved antioxidant capacity, and immunity while optimizing nutrient utilization and gut microbiota. The optimal dosage was determined to be 600–800 mg/kg. These findings suggest that OSA serves as a promising antimicrobial alternative in piglet farming. Full article

As a traditional Chinese herbal medicine, Cannabis sativa holds broad prospects for application in the development of functional foods, pharmaceutical formulations, dietary supplements, and cosmetic products. However, the bioactivity of polysaccharides in C. sativa has been largely overlooked. In this study, crude C. sativa leaf polysaccharide (CSLP) was extracted using the hot-water extraction and ethanol-precipitation method. CSLP contains 64.15 ± 1.96% carbohydrates and 2.13 ± 0.47% protein, with a yield of 6.71 ± 0.84% (w/w). Preliminary structural characterization showed that CSLP was mainly composed of arabinose, galactose, and glucose, with a molecular weight of 28.867 kDa. CSLP not only demonstrated potential in vitro antioxidant activity against ABTS, DPPH, superoxide anion, and hydroxyl radicals, but also repaired H₂O₂-induced oxidative damage in RAW 264.7 macrophages by increasing the cellular levels of SOD, CAT, and GSH-Px, and reducing MDA levels. Mechanistically, CSLP possibly modulated the Nrf2/Keap1 signaling pathway in H₂O₂-stimulated RAW 264.7 cells via upregulating the gene expressions of Nrf2, NQO1, and HO-1, while downregulating Keap1 expression. These results suggest that CSLP could potentially be used as an antioxidant ingredient in the food, pharmaceutical, and cosmetic industries. Full article