Expression Of Superoxide Dismutase Research Articles

Chitosan Nanoparticle-Encapsulated Cordyceps militaris Grown on Germinated Rhynchosia nulubilis Reduces Type II Alveolar Epithelial Cell Apoptosis in PM2.5-Induced Lung Injury

Chitosan nanoparticles (CNPs) were synthesized in this study to enhance the limited bioactivity and stability of Cordyceps militaris grown on germinated Rhynchosia nulubilis (GRC) and effectively deliver it to target tissues. Under optimized conditions, stable encapsulation of GRC was achieved by setting the chitosan (CHI)-to-tripolyphosphate (TPP) ratio to 4:1 and adjusting the pH of TPP to 2, resulting in a zeta potential of +22.77 mV, which indicated excellent stability. As the concentration of GRC increased, the encapsulation efficiency decreased, whereas the loading efficiency increased. Fourier-transform infrared (FT-IR) spectroscopy revealed shifts in the amide I and II bands of CHI from 1659 and 1578 to 1639 cm⁻1, indicating hydrogen bonding and successful encapsulation of GRC encapsulated with CNPs (GCN). X-ray diffraction (XRD) examination revealed the transition of the nanoparticles from a crystalline to an amorphous state, further confirming successful encapsulation. In vivo experiments demonstrated that GCN treatment significantly reduced lung injury scores in fine particulate matter (PM2.5)-exposed mice (p < 0.05) and alleviated lung epithelial barrier damage by restoring the decreased expression of occludin protein (p < 0.05). In addition, GCN decreased the PM2.5-induced upregulation of MMP-9 and COL1A1 mRNA expression levels, preventing extracellular matrix (ECM) degradation and collagen accumulation (p < 0.05). GCN exhibited antioxidant effects by reducing the mRNA expression of nitric oxide synthase (iNOS) and enhancing both the protein and mRNA expression of superoxide dismutase (SOD-1) caused by PM2.5, thereby alleviating oxidative stress (p < 0.05). In A549 cells, GCN significantly reduced PM2.5-induced reactive oxygen species (ROS) production compared with GRC (p < 0.05), with enhanced intracellular uptake confirmed using fluorescence microscopy (p < 0.05). In conclusion, GCN effectively alleviated PM2.5-induced lung damage by attenuating oxidative stress, suppressing apoptosis, and preserving the lung epithelial barrier integrity. These results emphasize its potential as a therapeutic candidate for preventing and treating the lung diseases associated with PM2.5 exposure.

Investigation of the Mechanism of Pachyman against Gout Arthritis with Network Pharmacology Analysis and Verification In Vivo.

Pachyman, derived from Poria cocos, has been used to treat gouty arthritis (GA) for thousands of years, although its precise role and mechanisms remain unclear. Herein, we investigate the therapeutic effects of pachyman on GA and explore their underlying mechanisms. Network pharmacology and experimental methods were employed to investigate the therapeutic mechanisms of pachyman against GA. The protein-protein interaction network of shared targets between pachyman and gout was constructed. Furthermore, we elucidated the functions and mechanisms of pachyman against GA. Subsequently, we validated the predicted mechanisms from an experiment on rats. The treatment of GA with pachyman primarily related to tumor necrosis factor (TNF), matrix metalloproteinases (MMP), and relaxation factor signaling pathways. In the experimental validation, pachyman were found to regulate the expression of IL-1β, TNF-α, TGF-β, superoxide dismutase, and glutathione peroxidase of hyperuricemic rats. These collective findings suggest that pachyman holds promise as an alternative treatment for GA.

PPARγ activation attenuates neonatal CRD-induced visceral pain sensitization and anxiety in male rats by alleviating oxidative stress

BackgroundVisceral pain sensitization and emotional reactions due to irritable bowel syndrome (IBS) occur frequently in the general population. Oxidative stress plays a crucial role in the pathogenesis of IBS. Previous studies have demonstrated that activation of peroxisome proliferator-activated receptor gamma (PPARγ) has analgesic effects. Therefore, we aimed to determine whether PPARγ activation ameliorates oxidative stress and affects thus nociceptive sensitization and emotional responses in IBS.MethodsThe study utilized male Sprague-Dawley (SD) rats, that suffered from neonatal colorectal distension (CRD), to assess the effects of various doses of rosiglitazone on visceral hyperalgesia and anxiety. Electromyography (EMG) of the external abdominal oblique muscles was used to evaluate visceral hypersensitivity, and Open Field Test (OFT) and Elevated Plus Maze (EPM) were used to evaluate anxiety. Superoxide dismutase (SOD) and malondialdehyde (MDA) in the spinal cord were analyzed by water-soluble tetrazolium-1 (WST-1) and thiobarbituric acid (TBA) methods, respectively, the expression levels of PPARγ in the spinal cord were assessed by qRT-PCR and Western blotting.ResultsNeonatal CRD-induced rats showed visceral pain sensitization and anxiety in adulthood, with down-regulated expression of PPARγ and SOD and elevated MDA levels in the spinal cord. Rosiglitazone alleviated visceral hypersensitivity and anxiety by activating PPARγ protein expression and promoting MDA up-regulation and SOD down-regulation in the spinal cord, which were reversed by GW9662, an antagonist of PPARγ.ConclusionThis study demonstrated that rosiglitazone alleviated visceral pain sensitization and anxiety in male IBS rats by alleviating oxidative stress through activation of PPARγ.

N-acetyl-L-cysteine and lauric acid; effective antioxidant and antimicrobial feed additives for juvenile Pacific white shrimp (Litopenaeus vannamei) cultured at high stocking density.

Present study aimed at improving the immune and antioxidant response of Pacific white shrimp (Litopenaeus vannamei) cultured at high stocking density fed with 0.2% supplementation of lauric acid (LA) and N-acetyl-L-cysteine (NAC). Shrimp (initial average weight = 0.65 g; n = 270) were grown at low stocking density (LSD) (n = 10/0.80 ft3 per replicate) and high stocking density (HSD) (n = 20/0.80 ft3 per replicate). They were randomly distributed into five groups (T1: negative control at LSD, T2: positive control at HSD, T3: at HSD and fed with LA supplement diet, T4: at HSD and fed with NAC supplemented diet, T5: at HSD and fed with combination of LA and NAC). All these five treatments were studied in triplicates and study continued for eight weeks. Better growth and higher levels of glucose, total protein, total hemocyte count and phagocytic index were observed in shrimp fed with NAC and LA supplemented diets. Observed survival rate and feed conversion ratio in all treatments was 75-89% and < 0.82, respectively. All parameters indicating stress were observed to be higher in T1 as compared to T2. Improved expression of superoxide dismutase and glutathione peroxidase and lower levels of malondialdehyde genes in T3, T4 and T5 showed that supplementation with these nutraceuticals can improve antioxidant response at high stocking density. A parallel increase was observed in the profiles of prophenoloxidase and lysozyme, underscoring the immune-boosting effects of both NAC and LA. This finding was further supported by higher expression of innate immune signaling pathway-related gene, toll like receptor-2 in T3, T4 and T5. In conclusion, NAC and LA, can possibly improve the resistance of white pacific shrimp against oxidative stress and pathogens when cultured in intensive production system.

Putative effects of moringa oil or its nano-emulsion on the growth, physiological responses, blood health, semen quality, and the sperm antioxidant-related genes in ram

Phytochemicals have been effectively used to enhance the growth and productivity of farm animals, while the potential roles of essential oils and their nano-emulsions are limited. This plan was proposed to investigate the impacts of orally administered moringa oil (MO) or its nano-emulsion (NMO) on the growth, physiological response, blood health, semen attributes, and sperm antioxidant-related genes in rams. A total of 15 growing Rahmani rams were enrolled in this study and allotted into three groups. The 1st control group received a basal diet only and treated orally one mL of distilled water, while the 2nd, and 3rd groups received a basal diet and were orally treated with 1 mL of NMO or 2 mL of MO /head/day for 4 months, respectively. Growth, physiological response, blood health, semen quality, and antioxidant genes in sperm were assessed. The MO and NMO treatments had no significant effect on growth indices (final body weight and weight gain ) and physiological response (rectal temperature, pulse, and respiration rates) (P > 0.05). The NMO group had the lowest levels of MCV (mean corpuscular volume) (P < 0.05), while all treated groups produced higher levels of mean corpuscular hemoglobin (MCH) and mean corpuscular hemoglobin concentration (MCHC) compared to those in the control group (P < 0.05). Aspartate transferase (AST) and total cholesterol were significantly reduced in the MO and NMO groups, while total protein and glucose levels were significantly improved in NMO group (P < 0.05). Serum and seminal interstitial-cell-stimulating hormone (ICSH) levels were significantly improved (P < 0.0001) in the NMO group. Testosterone in serum and seminal plasma was significantly improved (P < 0.0001) in the MO group. Total antioxidant capacity (TAC) levels showed a tendency to increase in both the MO and NMO groups, but this increase was not significant compared to the untreated group (P > 0.05). On the other hand, the MO group exhibited lower levels of AST and malondialdehyde (MDA), while the alanine aminotransferase (ALT) levels were the lowest in the NMO group (P > 0.05). Mass motility, viability, membrane integrity and sperm concentration were significantly improved in the MO group (P < 0.0001) compared to the other groups. The NMO group had worse expressions of superoxide dismutase 1 (SOD1) compared to the control and MO groups. MO group significantly upregulated the catalase gene compared to the other groups (P < 0.001). The expression of Caspase-3 was highest in the group that received NMO compared to the other groups (P < 0.001). This study suggests that MO may serve as a novel therapeutic agent for improving the reproductive health in Rahmani rams.

Amyotrophic lateral sclerosis caused by SOD1 variants: from genetic discovery to disease prevention.

Pathogenic variants in the superoxide dismutase 1 (SOD1) gene were the first identified genetic cause of amyotrophic lateral sclerosis (ALS), in 1993. This discovery enabled the development of transgenic rodent models for studying the biology of SOD1 ALS. The understanding that SOD1 ALS is driven by a toxic gain-of-function mutation has led to therapeutic strategies that aim to lower concentrations of SOD1 protein, an endeavour that has been complicated by the phenotypic heterogeneity of SOD1 ALS. The successful development of genetically targeted therapies to reduce SOD1 expression, together with a better understanding of pre-symptomatic disease and the discovery of neurofilament light protein as a susceptibility/risk biomarker that predicts phenoconversion, has ushered in a new era of trials that aim to prevent clinically manifest SOD1 ALS. The 30-year journey from gene discovery to gene therapy has not only uncovered the pathophysiology of SOD1 ALS, but has also facilitated the development of biomarkers that should aid therapy development for all forms of ALS.

Exosome-equipped TNF antisense oligodeoxynucleotide or 2-deoxy-D-glucose ameliorated nonalcoholic steatohepatitis by modulating superoxide dismutase 1 in mice.

Inflammatory mediators tumor necrosis factor (TNF) and interleukin 1 beta (IL1β), primarily derived from hepatic macrophages in the liver, play a crucial role in the progression of nonalcoholic steatohepatitis (NASH). Meanwhile, intravenously injected exosomes are mainly distributed in the liver and predominantly taken up by hepatic macrophage. Herein, we aimed to evaluate the feasibility of targeted inhibition of TNF and IL1β expression in hepatic macrophages via exosomes as a potential therapeutic strategy for NASH. In this study, we demonstrated that antisense oligodeoxynucleotide targeting TNF (ASO-TNF) or 2-deoxy-d-glucose (2DG) effectively suppressed the expression of TNF and/or IL1β in macrophages. Exosomes loaded with ASO-TNF or 2DG were able to suppress the expression of TNF and/or IL1β in macrophages in vitro or in vivo. Furthermore, infusion of Exo/ASO-TNF or Exo/2DG significantly attenuated experimental steatohepatitis in choline deficient amino acid-defined (CDAA) or methionine and choline deficient (MCD) diet-fed mice. RNA-seq results showed that treatment with Exo/ASO-TNF or Exo/2DG significantly inhibited pro-inflammatory signaling pathways. Mechanistically, we observed that administration of Exo/ASO-TNF or Exo/2DG could attenuate NASH progression by up-regulating the expression of superoxide dismutase 1 (Sod1). Combined, our findings demonstrated that infusion of exosomes loaded with ASO-TNF or 2DG alleviated experimental steatohepatitis in murine models. Thus, infusion of exosomes loaded with anti-inflammatory agents holds promise as a potential therapeutic strategy for NASH treatment.

Phytic Acid Delays the Senescence of Rosa roxburghii Fruit by Regulating Antioxidant Capacity and the Ascorbate-Glutathione Cycle.

Rosa roxburghii fruit has a short postharvest shelf life, with rapid declines in quality and antioxidant capacity. This research assessed how phytic acid affects the antioxidant capacity and quality of R. roxburghii fruit while in the postharvest storage period and reveals its potential mechanism of action. The findings suggested that phytic acid treatment inhibits the production of malondialdehyde (MDA) and enhances the activities and expressions of glutathione peroxidase (GPX), peroxidase (POD), catalase (CAT), and superoxide dismutase (SOD) while decreasing the generation of superoxide anions (O2•-) and hydrogen peroxide (H2O2). Phytic acid treatment activates the ascorbate-glutathione (AsA-GSH) cycle and enhances the activity and expression of key enzymes in the cycle: ascorbate peroxidase (APX), glutathione reductase (GR), dehydroascorbate reductase (DHAR), and monodehydroascorbate reductase (MDHAR). It also increases the levels of non-enzymatic antioxidants, such as ascorbic acid (AsA) and glutathione (GSH), while reducing the production of dehydroascorbic acid (DHA) and oxidized glutathione (GSSG). Moreover, phytic acid treatment enhances the ratios of AsA/DHA and GSH/GSSG, maintaining the reduced state of the fruit. In summary, phytic acid improves antioxidant defense system and activates the AsA-GSH cycle, alleviating oxidative damage and ensuring R. roxburghii fruit quality after harvest.

Alpha-synuclein expression in neurons modulates Japanese encephalitis virus infection.

Japanese encephalitis virus (JEV) poses a significant threat, particularly to children. Despite extensive research efforts, the development of effective treatments against JEV has been impeded. One of the major setbacks is a lack of comprehensive understanding of neurotropism. The study focuses on alpha-synuclein (α-syn), a neuronal protein, and aims to determine its role in JEV pathogenesis. The present study reveals that the host cell upregulates α-syn in response to JEV infection. α-syn restrains JEV propagation by modulating superoxide dismutase 1 (SOD1) expression which further blocks JEV-induced ROS generation. Endogenous α-syn silencing led to a decrease in SOD1 expression and increased viral titer. α-syn plays a crucial role in counteracting oxidative stress through SOD1, which is essential for limiting JEV replication. This study provides broader implications for antiviral strategies and their possible role in neurodegenerative diseases; however, there is still much to explore, particularly regarding α-syn aggregation kinetics in JEV infection.

Bacillus amyloliquefaciens Regulates the Keap1/Nrf2 Signaling Pathway to Improve the Intestinal (Caco-2 Cells and Chicken Jejunum) Oxidative Stress Response Induced by Lipopolysaccharide (LPS).

This article aims to investigate the mechanism by which Bacillus amyloliquefaciens alleviates lipopolysaccharide (LPS)-induced intestinal oxidative stress. The study involved two experimental subjects: human colorectal adenocarcinoma (Caco-2) cells and Arbor Acres broiler chickens. The experiment involving two samples was designed with the same treatment groups, specifically the control (CK) group, lipopolysaccharide (LPS) group, Bacillus amyloliquefaciens (JF) group, and JF+LPS group. In the Caco-2 experiment, we administered 2 μg/mL of LPS and 1 × 106 CFU/mL of JF to the LPS and JF groups, respectively. In the broiler experiment, the LPS group (19-21 d) received an abdominal injection of 0.5 mg/kg BW of LPS, whereas the JF group was fed 1 × 107 CFU/g of JF throughout the entire duration of the experiment (1-21 d). The results indicated the following: (1) JF significantly decreased the DPPH free radical clearance rate and hydrogen peroxide levels (p < 0.05). (2) JF significantly enhanced the total antioxidant capacity (T-AOC), superoxide dismutase (SOD), and glutathione peroxidase (GSH Px) activity in Caco-2 cells (p < 0.05), while concurrently reducing malondialdehyde (MDA) content (p < 0.05). (3) Compared to the CK group, JF significantly increased the mRNA expression levels of nuclear factor-erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), SOD, catalase (CAT), GSH-Px, interleukin-4 (IL-4), interleukin-10 (IL-10), Claudin, Occludin1, zonula occludens-1 (ZO-1), and mucin 2 (MUC2) in Caco-2 cells (p < 0.05), while concurrently reducing the mRNA expression of Kelch-like ECH-associated protein 1 (Keap1), tumor necrosis factor-alpha (TNF-α), interleukin-1β (IL-1β), and interleukin-8 (IL-8) (p < 0.05). In comparison to the LPS group, the JF+LPS group demonstrated a significant increase in the mRNA expression of Nrf2, SOD, GSH-Px, and IL-4, as well as Occludin1, ZO-1, and MUC2 in Caco-2 cells (p < 0.05), alongside a decrease in the mRNA expression of Keap1, TNF-α, and IL-1β (p < 0.05). (4) In broiler chickens, the JF group significantly elevated the levels of T-AOC, CAT, and GSH-Px in the jejunum while reducing MDA content (p < 0.05). Furthermore, the CAT level in the JF+LPS group was significantly higher than that observed in the LPS group, and the levels of MDA, TNF-α, and IL-1β were significantly decreased (p < 0.05). (5) In comparison to the CK group, the JF group exhibited a significant increase in Nrf2 levels in the jejunum of broiler chickens (p < 0.05). Notably, the mRNA expression levels of IL-4, IL-10, Claudin, Occludin1, ZO-1, and MUC2 were reduced (p < 0.05), while the mRNA expression levels of Keap1, TNF-α, and IL-1β also showed a decrease (p < 0.05). Furthermore, the mRNA expression levels of Nrf2, Occludin1, ZO-1, and MUC2 in the JF+LPS group were significantly elevated compared to those in the LPS group (p < 0.05), whereas the mRNA expression levels of Keap1 and TNF-α were significantly diminished (p < 0.05). In summary, JF can enhance the intestinal oxidative stress response, improve antioxidant capacity and intestinal barrier function, and decrease the expression of inflammatory factors by regulating the Keap1/Nrf2 signaling pathway.

Metabolism and immune responses of striped hamsters to ectoparasite challenges: insights from transcriptomic analysis.

The striped hamster, often parasitized by ectoparasites in nature, is an ideal model for studying host-ectoparasite molecular interactions. Investigating the response to ectoparasites under laboratory conditions helps elucidate the mechanism of host adaptations to ectoparasite pressure. Using transcriptome sequencing, we analyzed gene expression in striped hamsters after short-term (3 days) and long-term (28 days) flea (Xenopsylla cheopis) parasitism. Differentially expressed genes (DEGs) were identified and subjected to Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Hub genes were pinpointed using protein-protein interaction (PPI) network analysis and the MCODE in Cytoscape. Gene Set Enrichment Analysis (GSEA) was used to further clarify the functional pathways of these hub genes. Validation of DEGs was performed via RT-qPCR. Additionally, the concentrations of reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were determined using specific enzyme-linked immunosorbent assay (ELISA) detection kits for hamsters. GO analysis revealed that during early parasitism, hosts primarily responded to the ectoparasites by adjusting the expression of genes related to metabolic functions. As parasitism persisted, the immune response became prominent, activating various immune pathways against ectoparasites. KEGG analysis confirmed the ongoing roles of metabolism and immunity. Notably, the chemical carcinogenesis - reactive oxygen species pathway was upregulated during flea parasitism, with downregulation of hub genes ATP5MC1 and ATP5MC2, highlighting the importance of mitochondrial function in oxidative stress. ELISA findings revealed that on day 3, flea parasitism groups showed elevated ROS expression and reduced SOD and CAT levels compared to the control group. By day 28, only SOD expression showed a significant decrease in both parasitism groups. This study uncovered the dynamic changes in metabolism and immune responses of striped hamsters parasitized by Xenopsylla cheopis. Hosts adjust their physiological and immune states to optimize survival strategies during different ectoparasite stages, enhancing our understanding of host-ectoparasite interactions. This also paves the way for further research into how hosts regulate complex biological processes in response to ectoparasite challenges.

Transcriptomic Study of Nicotiana tabacum Treated with the Bacterial Protein CspD Reveals Some Specific Abiotic Stress Responses.

The ability of a cold-shock protein CspD from Bacillus thuringiensis to protect both dicots and monocots against various pathogens is well confirmed under both greenhouse and field conditions; however, the molecular basis of this phenomenon at the transcriptomic level still remains unexplored. Expression profiles of some marker genes associated with SAR/ISR nonspecific resistance pathways and ROS scavengers were examined in CspD-treated Nicotiana tabacum plants, and the RNA-seq analysis of CspD-treated plants was first carried out. The ISR markers PDF1.2 and PR4 were overexpressed locally in treated tobacco leaves with the maximum 2.4- and 5.7-fold change, respectively, reached 12 h after the leaf treatment with CspD; PDF1.2 was also up-regulated 4.8-fold four days after the inoculation of treated plants with TMV. The ROS scavenger analysis demonstrated overexpression of Cu-Zn superoxide dismutase in both treated (with the maximum 5.4-fold change observed 6 h after the treatment) leaves and leaves from the upper tier ("system" leaves, 6.5-fold change observed 4 days after the treatment). The ROS assay confirmed endogenous accumulation of superoxide in CspD-treated leaves 6 and 24 h after the treatment. An in silico comparative study of Arabidopsis orthologs of highly up-regulated tobacco genes induced by CspD with Arabidopsis genes activated by some other molecular patterns revealed the specific CspD-induced expression of Cu-Zn superoxide dismutase and some other genes associated with light and cold responses. This study may contribute to a better understanding of cross-talking between abiotic stress and nonspecific immunity in plants.

Protective Effects of NRF2 Activator Sulforaphane in Polyinosinic:Polycytidylic Acid-Induced In Vitro and In Vivo Model.

NRF2 is a nuclear transcription factor involved in the cellular protection against oxidative stress and inflammatory signaling. Sulforaphane is a known NRF2 activator used for its strong antioxidant and anti-inflammatory activity through regulation of Keap-1-HO-1 pathway. However, there is a limited exploration about the role of NRF2 activator, sulforaphane in regulation of poly(I:C)-induced oxidative stress, inflammation and injury in lung. Therefore, we aimed to evaluate the therapeutic effect of sulforaphane in poly(I:C)-induced responses using in vitro as well as in vivo model. We evaluated oxidative stress and inflammatory cytokines in poly(I:C)-induced RAW264.7 cells. We also employed in vivo animal study to evaluate tissue oxidative-antioxidative balance along with expression of NRF2, Keap-1, histopathological assessment by hematoxylin-eosin staining and picrosirius red staining to explore the protective mechanisms of sulforaphane in poly(I:C)-induced mouse model. Our results indicated that sulforaphane increased the expression of NRF2 and its downstream proteins. In addition, sulforaphane alleviated poly(I:C)-induced activation of the oxidative and pro-inflammatory pathways, histopathological changes, depleted expression of GSH and superoxide dismutase in lung tissue. This study suggested that sulforaphane may be one of the useful therapeutic alternatives for poly(I:C) induced lung injury and inflammation.

Dapagliflozin has protective effects on palmitate-induced renal tubular epithelial cells by enhancing mitochondrial function and reducing oxidative stress.

Sodium-glucose co-transporter 2 (SGLT2) inhibitors, commonly utilized for diabetic nephropathy, have demonstrated benefits beyond glucose control, including organ protection. This study investigated the protective effects of the SGLT2 inhibitor, dapagliflozin (DAPA), on palmitate-induced renal tubular epithelial cell (HK-2) injury, particularly concentrating on mitochondrial function and oxidative stress. HK-2 cells were treated with 150μmol/L palmitate to induce mitochondrial dysfunction and oxidative stress, and they were co-treated with 2μmol/L DAPA for 24h. DAPA significantly increased cell viability (P<0.05), reduced reactive oxygen species (ROS) levels (P<0.001), and restored mitochondrial membrane potential (P<0.05). It also lowered malondialdehyde (MDA) level (P<0.001) and increased superoxide dismutase (SOD) expression level (P<0.001). Western blot analysis revealed that DAPA reversed palmitate-induced upregulation of apoptosis-related proteins, including Bax and Cytochrome C. DAPA also mitigated the overactivation of autophagy-related proteins, such as LC3 and Beclin-1, indicating its role in modulating autophagy under diabetic nephropathy. Electron microscopy confirmed improvements in mitochondrial morphology, accompanying by reduced swelling and restored cristae structure. These findings highlight the potential of DAPA, as an SGLT2 inhibitor, to mitigate renal injury by enhancing mitochondrial function and reducing oxidative stress, providing novel insights into its therapeutic value for diabetic nephropathy management.

Assessment of Placental Antioxidant Defense Markers in Vaccinated and Unvaccinated COVID-19 Third-Trimester Pregnancies.

Pregnancy has been identified as a risk factor for severe COVID-19, leading to maternal and neonatal complications. The safety and effects of the SARS-CoV-2 vaccination during pregnancy, particularly on placental function and oxidative stress (OxS), remain underexplored. We investigated the impact of vaccination on third-trimester placental antioxidant defense markers. Ninety full-term pregnant women were divided into the following groups: vaccinated (n = 27) and unvaccinated (n = 25) COVID-19-positive pregnant women; control subgroups were composed of vaccinated (n = 19) or unvaccinated (n = 19) COVID-19-negative women with a healthy term singleton pregnancy with no signs of COVID-19. Placental samples were collected after delivery. Lipid peroxidation (TBARS), gene expression of HIF-1α, and catalase (CAT), superoxide dismutase-1 (SOD1) and CAT-SOD1 enzymatic activity were measured. COVID-19-positive placentae exhibited significantly higher TBARS and HIF-1α levels compared to controls, regardless of vaccination status. Vaccination significantly increased placental CAT and SOD1 expression and activity in COVID-19-positive women, suggesting enhanced antioxidant defense. Unvaccinated women showed a higher incidence of COVID-19 symptoms and lower antioxidant enzyme activity. SARS-CoV-2 infection induced placental OxS, which is countered by a placental adaptive antioxidant response. Vaccination during pregnancy enhances placental defense, further supporting the safety and benefits of COVID-19 vaccination in preventing complications and protecting fetal development.

Stimulatory effects of dietary savory (Satureja hortensis L.) ethanolic extract on growth, digestive enzymes, immune parameters, antioxidant defense, and immune and antioxidant-related genes in zebrafish (Danio rerio)

The current investigation focused on examining the growth performance, immune and antioxidative factors, and mRNA levels of immune and antioxidant-related genes in zebrafish (Danio rerio) that were fed with different levels of savory (Satureja hortensis L.) ethanolic extract (SEE) for 8 weeks. To achieve this objective, a total of 240 zebrafish with a mean weight of 65.37 ± 5.9 mg were fed on 0.0 (the control; T0), 0.5 % (T0.5), 1 % (T1), and 2 % (T2) of SEE for a period of 8 weeks. The results for the growth performance of zebrafish showed that the final weight (165.20±1.92 mg), Weight gain (147.71±1.15 mg), specific growth rate (1.62±0.03) was significantly (P < 0.05) enhanced with the dietary SEE levels and the best performance was noted in T1 and T2. highest activity levels of α-amylase (53.56±1.21), lipase (3.56±0.16), proteases (13.78±0.21), pepsin (0.31±0.01), chymotrypsin (0.44±0.01), and trypsin (0.68±0.01) were observed especially T2 (P < 0.05). The results of tissue and mucus immune factors revealed that feeding the fish on SEE diets significantly increased the immune activity represented by lysozyme, total Immunoglobulin (Ig), Immunoglobulin M (IgM), total protein, and ACH50 (P < 0.05). The malondialdehyde value was significantly (P < 0.05) affected by experimental diets and its lowest value was notably observed in T1 and T2 than those in T0 and T0.5. The tissue and mucus activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and total antioxidant activity (TAC) increased considerably (P < 0.05) in the treatments fed with SEE, and their highest levels were detected in T1 and T2. The relative mRNA expression of CAT, SOD, GPx, and glutathione reductase (GSR) genes in treatments fed with different SEE levels was higher than those in the control group. The relative expression of Lysozyme was notably higher, meanwhile the expression of genes including Interleukin 1β (IL.1B), Interleukin 8 (IL8), and Tumor necrosis factor (TNF-α), significantly decreased in fish fed with SEE; especially at T1 and T2. The present study, 1–2 % savory ethanolic extract of SEE improved the performance, immune, and antioxidant levels.

High Dietary Zinc Promotes its Optimal Absorption Through Modulation of Key Transporter Genes, SOD1, and HSP70 Expression in Heat-stressed Rats.

Global warming causes heat stress (HS) in animals, impacting nutrient absorption and metabolism. Antioxidant nutrients are crucial for combating HS. This study assessed the impact of increased dietary Zn on nutrient utilization, mineral absorption, and expression of Zn homeostasis regulators, superoxide dismutase-1 (SOD1), and heat shock protein-70 (HSP70) genes in rats under HS. Seventy-two four-week-old Wistar rats were assigned to six groups in a 3×2 factorial design, with three dietary Zn levels (14.6, 32.7, and 48.9 ppm) and two environments, thermo-neutral (TN) and HS, for 42 days, including 14 days of HS exposure. Results showed that HS reduced nutrient intake across Zn levels, though ether extract digestibility increased at 32.7 and 48.9 ppm Zn. Intake, excretion, and apparent daily absorption of Ca, P, Zn, Cu, Mn, and Fe were lower in HS than in TN groups. Hepatic metallothionein-1 (MT1) mRNA expression was downregulated in rats fed 14.6 and 32.7 ppm Zn compared to 48.9 ppm Zn under both environmental conditions. Duodenal Zinc transporter-1 (ZnT1) and Zrt- and Irt-like protein-1 (ZIP1) mRNA expression increased with dietary Zn under TN and HS conditions, respectively. Hepatic SOD1 mRNA expression was significantly downregulated in HS groups, while hepatic HSP70 mRNA expression was significantly upregulated at 48.9 ppm Zn under HS. Present study suggests that, under HS conditions in rats, a higher dietary Zn level of 48.9 ppm may be optimal for improving Zn absorption, enhancing ZIP1, MT1, and HSP70 gene expression, and alleviating the negative effects of HS.

Liposome encapsulating pine bark extract in Nile tilapia: Targeting interrelated immune and antioxidant defense to combat coinfection with Aeromonas hydrophila and Enterococcus faecalis

Application of smart delivery systems for encapsulation of natural ingredients provides novel avenues and is being frequently developed. Thus, we aimed to highlight the effects of cyclosome liposomal pine bark extract (CL-PBE) on Nile tilapia growth, immunomodulation, antioxidant capacity and resistance against coinfection with Aeromonas hydrophila and Enterococcus faecalis and their associated virulence genes. The experiment was conducted on four fish groups receiving a control diet (control) along with three baseline meals supplemented with 200, 400 and 600 mg/kg diet of CL-PBE (CL-PBE 200, 400 and 600, respectively). At the end of the 12-weeks feeding trial, the tilapias were intraperitoneally challenged with virulent A. hydrophila strain and five days later, E. faecalis challenge was carried out. The results revealed that tilapias fed diets fortified with CL-PBE displayed significantly enhanced growth rate and feed conversion ratio in a dose-dependent manner. Moreover, we demonstrated that CL-PBE had potent antioxidant property presented by modulation of several markers of oxidative stress; substantial reductions in reactive oxygen species, hydrogen peroxide and malondialdehyde levels, an elevation in total antioxidant capacity and boosting glutathione peroxidase (GSH-Px), catalase (CAT) and superoxide dismutase (SOD) activities in fish serum and muscle tissues. This was also correlated with augmenting the expression of CAT, SOD, GSH-Px, Nrf2 and caspase-1 genes alongside reducing those of COX-2, HSP70 and iNOS genes in response to CL-PBE. Our data demonstrated that CL-PBE fortification counteracted the overly pronounced inflammatory response-mediated induction of IL-1β, TNF-α, MHCII and TLR2 genes at the transcriptional levels post coinfection together with promotion in MUC2 and IL-10 genes expression. Notably, our findings displayed optimal well-functioning fish immune system post dietary supplementation of CL-PBE for the protection against coinfection with A. hydrophila and E. faecalis. This was evident from the decline of their counts and hence encompassing the capacity to reduce cumulative mortality percentage in conjunction with interference with their virulence via the significant downregulatory effects of CL-PBE on E. faecalis esp and gelE and A. hydrophila act and fla virulence genes. Taken together, our study strongly suggested dietary inclusion of CL-PBE for Nile tilapias with superior growth performance and significant economic benefits coupled with potent stimulatory effects on antioxidant capacity and immune response expediting our detailed understanding of how coinfection with A. hydrophila and E. faecalis was controlled.

Effects of hydrolyzed yeast on growth performance, intestinal redox homeostasis, and woody breast myopathy in heat-stressed broilers.

The objective of this study was to enhance the knowledge about the effects of hydrolyzed yeast supplementation on growth performance, woody breast myopathy, and its mechanism on intestinal homeostasis using antioxidant and immunomodulatory-related gene expressions in heat-stressed broiler chickens. In a 35-d feeding experiment, 160-day-old male Ross 308 broiler chickens were assigned to four dietary groups, consisting of eight replicates and five birds per replicate. Experimental diets contained four levels of hydrolyzed yeast (HY) (0, 400, 800, or 1,200 mg.kg-1) derived from Saccharomyces cerevisiae. On d 25, birds were exposed to cyclic heat stress (HS) (35°C for 8 h/d from 8 a.m. to 4.00 p.m.) for 10 days. Adding HY at 800 mg.kg-1 numerically decreased the feed conversion ratio (FCR) on days 25-35 (heat stress period) by 2.50%. Furthermore, the addition of HY reduced (P = 0.005) mortality rate compared with those of birds fed the control diet. Supplementation of HY exhibited efficacy (P = 0.09) in diminishing woody breast (WB) in terms of incidence and degree of severity. Furthermore, the added HY decreased (P < 0.001) drip loss values of the Pectoralis major compared with the control diet group; the addition of HY at 400 and 1,200 mg.kg-1 decreased (P < 0.001) cooking loss values in the Pectoralis major. In addition, HY supplementation at 800 mg.kg-1 decreased (P = 0.04) the duodenal mRNA expression of the avian β-defensin 10 (AvBD10) and increased (P < 0.05) the mRNA expression of nuclear factor erythroid 2-related factor 2 (Nrf2), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and secreted immunoglobulin A (sIgA). The addition of HY at 400 and 800 mg.kg-1 decreased (P = 0.001) the duodenal mRNA expression of copper and zinc superoxide dismutase (Cu-ZnSOD1). HY supplementation tended to decrease (P =0.07) the duodenal mRNA expression of heat shock protein 70 (HSP70). The results suggest that hydrolyzed yeast supplementation to broiler chickens exposed to heat stress might improve intestinal redox homeostasis and decrease the mortality rate. The inclusion of 800 mg.kg-1 HY in the diet enhanced duodenal redox homeostasis, while 400-1,200 mg.kg-1 HY reduced mortality rate and exhibited lower drip loss values and reduced woody breast of Pectoralis major in terms of incidence and degree of severity.

Cirsilineol improves anesthesia/surgery-induced postoperative cognitive dysfunction through attenuating oxidative stress and modulating microglia M1/M2 polarization.

Cirsilineol is a trimethoxy and dihydroxy flavonoid isolated from plant species such as Artemisia vestita and has a variety of pharmacological properties. This study analyzed whether cirsilineol could prevent postoperative cognitive dysfunction (POCD). A POCD mouse model induced by anesthesia/surgery induction and a cell model established with hydrogen peroxide (H2O2)-induced microglia BV-2 were employed to explore the efficacy of cirsilineol on POCD. The cognition function of the mice were assessed by carrying out behavioral tests (Morris water maze test and Y-maze test). We assessed the activation and polarization status of microglia using immunofluorescence analysis and detected the expression levels of CD86 and CD206 using the quantitative PCR (qPCR). Subsequently, cell viability was determined by CCK-8 assay and apoptosis was assessed using Calcein-AM/PI staining. Meanwhile, superoxide dismutase (SOD) and malondialdehyde (MDA) levels in plasma and cell culture medium were detected using chemiluminescence. Finally, the phosphorylation levels of JAK/STAT signaling pathway-related proteins were analyzed by Western blot. Cirsilineol reduced the escape latency and times of crossing island and increased spontaneous alternation (SA) rate, restoring the cognitive dysfunctions of POCD-modeled mice. Meanwhile, POCD elevated CD86 expression and malondialdehyde content and lowered the level of SOD; however, cirsilineol promoted CD206 expression and generation of SOD and inhibited malondialdehyde production. In H2O2-induced microglia BV-2, cirsilineol treatment increased SOD content and suppressed the generation of reactive oxygen species (ROS) and malondialdehyde, modulating microglia M1/M2 polarization and JAK/STAT pathway. Cirsilineol prevented against POCD by attenuating oxidative stress and modulating microglia M1/M2 polarization, providing novel insights for the management of POCD.