Upregulation Of Superoxide Dismutase Research Articles

Impact of Sublethal Insecticides Exposure on Vespa magnifica: Insights from Physiological and Transcriptomic Analyses

Insecticides are widely used to boost crop yields, but their effects on non-target insects like Vespa magnifica are still poorly understood. Despite its ecological and economic significance, Vespa magnifica has been largely neglected in risk assessments. This study employed physiological, biochemical, and transcriptomic analyses to investigate the impact of sublethal concentrations of thiamethoxam, avermectin, chlorfenapyr, and β-cypermethrin on Vespa magnifica. Although larval survival rates remained unchanged, both pupation and fledge rates were significantly reduced. Enzymatic assays indicated an upregulation of superoxide dismutase and catalase activity alongside a suppression of peroxidase under insecticide stress. Transcriptomic analysis revealed increased adenosine triphosphate-related processes and mitochondrial electron transport activity, suggesting elevated energy expenditure to counter insecticide exposure, potentially impairing essential functions like flight, hunting, and immune response. The enrichment of pathways such as glycolysis, hypoxia-inducible factor signaling, and cholinergic synaptic metabolism under insecticide stress highlights the complexity of the molecular response with notable effects on learning, memory, and detoxification processes. These findings underscore the broader ecological risks of insecticide exposure to non-target insects and highlight the need for further research into the long-term effects of newer insecticides along with the development of strategies to safeguard beneficial insect populations.

Ursolic Acid Restores Redox Homeostasis and Pro-inflammatory Cytokine Production in Denervation-Induced Skeletal Muscle Atrophy.

Skeletal muscle (SkM) atrophy results from metabolic disorders causing body and muscle mass loss, affecting morbidity and mortality. Increased oxidative stress, inflammation, and poor prognosis are the leading causes of involuntary weight loss. Ursolic acid (UA), known for its antioxidant and anti-inflammatory properties, can potentially reduce oxidative stress and inflammation in muscles, but its effects on muscle mass regulation are still unknown. Therefore, the present study investigated the medicinal efficacy of UA and its mode of action against the murine model of SkM atrophy over 7days of UA supplementation. Denervation-induced SkM atrophy significantly impacts overall body weight and the weight of individual muscles (p < 0.05). However, supplementation with UA can effectively counteract these effects by promoting the synthesis of the slow-myosin heavy chain, thereby restoring body weight and myotube diameter. Moreover, UA also plays a crucial role in reducing the production levels of reactive oxygen species (ROS), lipid peroxidation (LPO), and caspase-3-like activity in atrophied muscles. UA also prevents the leakage of creatine kinase (CK) through the upregulation of superoxide dismutase (SOD) and glutathione peroxidase (GPx) expression. Furthermore, the results obtained from qRT-PCR demonstrated a significant decrease in the levels of pro-inflammatory markers, namely IL-1β, IL-6, TNF-α, and TWEAK, up to four-fold after the third day of the UA intervention. UA also upregulated PGC-1α, Bcl2, and p-Aktser473 expression towards the regulation of redox homeostasis.

Superoxide dismutase 1 mediates adaptation to the tumor microenvironment of glioma cells via mammalian target of rapamycin complex 1

In glioblastoma (GB) cells oxidative stress is induced by both, conditions of the tumor microenvironment as well as by therapeutic interventions. Upregulation of superoxide dismutase 1 (SOD1), a key enzyme for oxidative defense and downstream target of mammalian target of rapamycin complex 1 (mTORC1) is a candidate mechanism to sustain survival and proliferation of tumor cells. SOD1 was inhibited by shRNA mediated gene suppression, CRISPR/Cas9 knockout and pharmacological inhibition in human (primary) GB cells. SOD1 activity was determined by SOD1/2 activity assay. ROS levels, cell death and the NADPH/NADP-ratio were measured under normal and starvation conditions. To study the mTORC1-SOD1 axis, mTORC1 activated TSC2 knockdown cells (TSC2sh) were analyzed. Genetic and pharmacological inhibition of SOD1 correlated with decreased SOD1 activity, increased ROS and enhanced the sensitivity of glioma cells towards starvation- and hypoxia-induced cell death. This was accompanied by a decreased NADPH/NADP-ratio. Furthermore, combination therapy of SOD1 and mTORC1 inhibition partially rescued the protective effect of mTORC1 inhibitor monotherapy. SOD1 mediates adaptation of GB cells to stress conditions in the tumor microenvironment in a mTORC1-dependent manner. Moreover, SOD1 activation contributes to the cell death resistance conferred by mTORC1 inhibitors under hypoxic conditions.

Resilient mechanism of strigolactone (GR24) in regulating morphological and biochemical status of maize under salt stress

Strigolactones (SLs), relatively recent plant growth regulators, bolster plant resilience in challenging environmental conditions and augment signaling networks. Salinity, a well-established abiotic stressor, threatens global crop cultivation and productivity. We hypothesized that the synthetic SL analogue GR24 could alleviate salinity stress in maize by reducing oxidative damage and enhancing various growth and physiological attributes. To explore this hypothesis, we subjected two maize hybrids, PB-ProA-2018 and PB-ProA-2019, to seed priming with three GR24 concentrations (non-soaked, water-soaked, 0.001, 0.01, 0.1 mg/L) for 16 h. Seeds were then germinated in sand culture under two salt stress levels [ 0 (Control) and 100 mM NaCl] and nourished with Hoagland's nutrient medium. Salt stress significantly stunted maize growth attributes. The pre-soaking seed treatment with 0.01 mg L⁻1 GR24 demonstrated a significant enhancement in plant growth metrics, yielding a 31.3% increase in root length and a 62% augmentation in total leaf area per plant, in comparison to non-soaked yet stressed plants. Salt stress led to increased activities of catalase and peroxidase, along with higher levels of leaf ascorbic acid, malondialdehyde, H₂O₂, glycine betaine, and free proline, compared to control seedlings. Pre-soaking with 0.01 mg L−1 GR24 further upregulated superoxide dismutase (SOD) by 29.6%, peroxidase (POD) by 68.3%, catalase (CAT) by 25%, ascorbic acid by 23.1%, free proline by 42.3%, and total phenolics content by 13%, compared to stressed counterparts. Notably, the 0.01 mg L−1 GR24 concentration exhibited superior efficacy in mitigating salt stress effects, with PB-ProA-2019 outperforming PB-ProA-2018 among the maize hybrids. These findings advance our understanding of SLs' potential in alleviating salinity stress in maize, offering valuable insights for crop resilience enhancement.

Resveratrol Mitigates Ischemia/Reperfusion-Induced Cardiomyocyte Injury by Inhibiting the Expression of Superoxide Dismutase 2

Resveratrol exhibits antioxidant, anti-inflammatory, and potentially cardio-protective properties. However, the effectiveness of resveratrol in acute myocardial infarction (AMI)-induced cardiomyocyte injury remains unclear. Superoxide Dismutase 2 (SOD2) is an important antioxidant enzyme in the mitochondria. However, few studies have reported the impact of SOD2 on AMI-induced cardiomyocyte injury. Therefore, we establish an in vitro model of cardiomyocyte ischemia/reperfusion (I/R) injury using oxygen-glucose deprivation/reoxygenation (OGD/R) to investigate the protective effects of resveratrol against OGD/R-induced cardiomyocyte injury and its underlying regulatory mechanism. Cell viability was assessed using the CCK-8. Apoptosis was evaluated by TUNEL staining. The levels of Cleaved cas-3, Bcl2, and SOD2 an important antioxidant enzyme in the mitochondria that is responsible for eliminating superoxide radicals were analyzed by western blot. The ROS positive rate was using a ROS/Superoxide detection assay kit. The relative abundance of the SOD2 mRNA was determined using the 2−ΔΔCT method. We demonstrated that OGD/R treatment significantly reduced AC16 cell viability while increasing apoptosis levels, oxidative stress, and inflammatory factor levels. We further confirmed the upregulation of SOD2 by OGD/R treatment, suggesting its potential involvement in modulating OGD/R-induced AC16 cell injury. Additionally, silencing SOD2 ameliorated the detrimental effects of OGD/R on AC16 cells. Moreover, we observed that upregulation of SOD2 aggravated OGD/R-induced AC16 cell injury, and resveratrol effectively reduced OGD/R-induced AC16 cell injury by down-regulating SOD2. In conclusion, this research provides a promising therapeutic strategy for mitigating I/R damage in AMI-induced cardiomyocytes, thereby identifying a potential target for therapeutic intervention.

Alpiniae oxyphyllae fructus improves production performance and egg quality of laying breeder hens by regulating reproductive hormones, antioxidant function, immunity and intestinal health

Alpiniae oxyphylla fructus was extensively utilized both as dietary supplements and traditional herbal medicines for healthcare functions and has exhibited a positive impact on animal health. The present study aimed to investigate the effects of Alpiniae oxyphyllae fructus powder (AOP) on production performance, egg quality, egg yolk fatty acid composition, reproductive hormones, antioxidant capacity, immunity, anti-apoptosis ability, and intestinal health in hens. A total of 252 Hainan Wenchang laying hens (30-wk-old) were randomly divided into 3 groups with 6 replicates, a basic diet with 0 (CON), 1 g/kg AOP (AOP1), and 3 g/kg (AOP3) mixed AOP. The AOP supplementation was found to decrease the feed conversion ratio and embryo mortality but to increase the laying rate, average egg weight, and oviduct index linearly (p < 0.05). Furthermore, AOP treatment reduced the total saturated fatty acids and palmitic acid (C16:0) in the egg yolk while increasing eggshell strength, albumen height, and Haugh unit (p < 0.05). The serum levels of albumin and phosphorus were increased, whereas total cholesterol, triglycerides, and glucose levels decreased as a result of AOP treatment (p < 0.05). The inclusion of 3 g/kg AOP had higher 17 β-estradiol and follicle-stimulating hormone levels in serum, while it up-regulated follicle-stimulating hormone receptor and gonadotropin-releasing hormone expression in ovary (p < 0.05). Dietary AOP strengthened the expression of nuclear factor erythroid2-related factor 2 in ovary and increased the activity of superoxide dismutase and total antioxidant capacity, but had a lower malondialdehyde content in serum (p < 0.05). AOP at 3 g/kg up-regulated superoxide dismutase 1 and heme oxygenase 1 expression in jejunum and ovary (p < 0.05). Meanwhile, AOP supplementation down-regulated p53 expression in ovary and bcl-2-associated x expression in liver and jejunum, especially 3 g/kg of AOP had lower caspase-8 concentrations and down-regulated bcl-2-associated x and caspase-3 expression in ovary (p < 0.05). AOP treatment increased serum levels of immunoglobulin A and immunoglobulin M and upregulated interleukin-4 expression in the liver, while decreasing interleukin-1β expression in liver and ovary and nod-like receptor protein 3 expression in jejunum (p < 0.05). Dietary AOP increased the ratio of villus height to crypt depth but decreased crypt depth in jejunum, especially when 1 g/kg AOP increased expression levels of occludin, mucin-2, peptide-transporter 1, and sodium glucose cotransporter 1 in jejunum (p < 0.05). AOP treatment altered the composition of the cecal microbial community, as evidenced by increased abundance of Oscillospira and Phascolarctobacterium and reduced richness of Clostridiaceae_Clostridium. Dietary AOP supplementation enriched lipid, amino acid, and propanoate metabolism. Spearman's correlation analysis revealed that the genera Oscillospira, Blautia, and Megasphaera were related to laying performance and intestinal integrity. In brief, supplementation of AOP, especially at 3 g/kg, could improve production performance and egg quality of hens via modulating reproductive hormones, antioxidant capacity, immunity, intestinal barrier, and cecal microbiota. Overall, the present work recommends the dietary inclusion of AOP as a beneficial additive for improving the performance of hens.

(-)-Epigallocatechin-3-O-Gallate Regulates Muscle Growth, Antioxidant Status, and Nutritional Composition of Juvenile Common Carp (Cyprinus carpio L.)

Among the polyphenolic compounds commonly found in green tea, (-)-epigallocatechin-3-gallate (EGCG) is known to have various functions, including the promotion of antioxidant and myofiber growth in mammals. However, the effect of EGCG on common carp (Cyprinus carpio L.) remains poorly understood. To evaluate the role of EGCG on juvenile common carp, 255 fish (initial weight 17.33 ± 0.34 g) were fed with five experimental diets containing 0, 0.05, 0.25, 0.5, and 1 g/kg EGCG. The results showed that diet supplementation with 0.05–0.5 g/kg EGCG supplementation significantly enhanced the specific growth rate (SGR) and reduced the feed conversion ratio (FCR). Weight gain rate (WGR) was significantly enhanced in the 0.25 and 0.5 g/kg EGCG groups. As for antioxidants, 0.25–1 g/kg EGCG significantly reduced protein carbonyl (PC) content and upregulated superoxide dismutase (sod) gene expression in the muscle. As for muscle nutritional composition, 0.05–0.5 g/kg EGCG increased total amino acid (TAA) and flavor amino acid (FAA) contents, likely via the rapamycin (mTOR) signaling pathway. Muscle n-3 polyunsaturated fatty acids (n-3 PUFA) content was increased with 0.5 g/kg EGCG, presumably owing to the upregulation of fatty acyl elongase 5 (elovl5), long-chain fatty acyl-CoA synthetase 6 (acsl6), and peroxisome proliferator-actiated receptor α (pparα). Dietary EGCG (0.05–1 g/kg) significantly increased muscle hardness and chewiness, accompanied by an increase in myofiber density. EGCG supplementation (0.25–1 g/kg) increased the pH value and reduced lactate contents in the muscle. However, muscle crude lipid and hydroxyproline contents significantly decreased with 1 g/kg EGCG. Overall, quadratic regression analysis of WGR, SGR, TAA, and FAA showed that optimal EGCG (0.46–0.52 g/kg) dietary supplementation improved the growth and nutritional composition of juvenile common carp.

Terpenoids derived from Semen Ziziphi Spinosae oil enhance sleep by modulating neurotransmitter signaling in mice

Semen Ziziphi Spinosae oil (SZSO) is a natural vegetable oil extracted from Semen Ziziphi Spinosae, a traditional Chinese medicine renowned for its sleep-promoting properties, while the mechanisms are still unclear. Our findings revealed that the terpenoids present in SZSO (T-SZSO) were identified as the active components responsible for promoting sleep. Network pharmacological analysis suggested that T-SZSO targeted different sleep-aid pathways to varying degrees and exhibited potential for preventing central nervous system diseases. Notably, lupeol and betulinicaldehyde exhibited more pronounced effects. Additionally, T-SZSO significantly elevated serotonin levels, enhanced gamma-aminobutyric acid (GABA) synthesis, promoted GABA A receptor expression, and decreased glutamate and norepinephrine expression levels. Moreover, T-SZSO was found to downregulate IL-1β expression while upregulating superoxide dismutase and inducible nitric oxide synthase levels. In conclusion, this study presents the first investigation into the pharmacological basis of SZSO in promoting sleep and highlights the potential of nature food in improving suboptimal health conditions.

Antioxidant and Anti-Inflammatory Properties of Quail Yolk Oil via Upregulation of Superoxide Dismutase 1 and Catalase Genes and Downregulation of EIGER and Unpaired 2 Genes in a D. melanogaster Model.

Quail egg yolk oil (QEYO) has a rich history of medicinal use, showcasing heightened antioxidant and bioactive properties in our prior studies. This positions QEYO as a promising candidate for therapeutic and cosmetic applications. In this investigation, QEYO was extracted using ethanol/chloroform and 2-propanol/hexane solvents. GC-MS and FTIR analyses quantified 14 major bioactive compounds in the ethanol/chloroform fraction and 12 in the 2-propanol/hexane fraction. Toxicity evaluations in fruit flies, spanning acute, sub chronic, and chronic exposures, revealed no adverse effects. Negative geotaxis assays assessed locomotor activity, while biochemical assays using fly hemolymph gauged antioxidant responses. Real-time PCR revealed the relative expression levels of the antioxidant and anti-inflammatory genes. FTIR spectra indicated diverse functional groups, and the GC-MS results associated bioactive compounds with the regulation of the anti-inflammatory genes EIGER and UPD2. While no significant change in SOD activities was noted, male flies treated with specific QEYO doses exhibited increased catalase activity and total antioxidant capacity, coupled with a significant decrease in their malondialdehyde levels. This study offers valuable insights into the bioactive compounds of QEYO and their potential regulatory roles in gene expression.

Umbilical Cord Blood-Derived Cells Can Reconstruct Hematopoiesis in an Aplastic Anemia Animal Model.

To explore the efficacy and the mechanism of the umbilical cord-derived cells combined with cyclosporine A (CsA) in treating aplastic anemia (AA) in mice. Immune-mediated AA model mice were treated with CsA + UC mesenchymal stem cells (UC-MSC), CsA + umbilical cord blood regulatory T cells (UCB-Treg), UC-MSC, UCB-Treg, CsA alone, or blank control, respectively (n = 9 mice/group). CsA and the cell infusion was administered on d0. Routine peripheral blood testing was performed once weekly; bone marrow colony culture, bone marrow cell flow cytometry, peripheral blood T cell subsets, and serum inflammatory cytokines tests were performed on d14. Transcriptome sequencing was performed for cells from CsA + UC-MSC, CsA + UCB-Treg, and CsA groups to detect the possible related genes. Gene function cluster and signal pathway enrichment analysis were also performed. Blank control mice died due to pancytopenia within 21 days, whereas mice in other groups survived for >28 days. On d14, the CsA + UC-MSC and CsA + UCB-Treg groups had higher white blood cell (WBC) counts than the other groups (p < 0.05), along with higher burst-forming unit (BFU) and colony-forming unit-granulocyte, macrophage (CFU-GM) counts (p < 0.01). The CsA + UC-MSC group had the highest BFU count (p < 0.01). The CsA + UC-MSC and CsA + UCB-Treg groups exhibited the highest bone marrow CD34+ cell proportion (9.68% ± 1.35% and 8.17% ± 0.53%, respectively; p < 0.01). Tumor necrosis factor (TNF)-α and interleukin (IL)-2 levels in the CsA + UC-MSC group (p < 0.05) and TNF-α, interleukin-2, and interferon (INF)-γ levels in the CsA + UC-Treg group (p < 0.01) were lower than those in the CsA group. Compared with CsA treatment, CsA + UC-MSC significantly downregulated the histone methylation pathway (p < 0.05), whereas CsA + UCB-Treg significantly upregulated energy metabolism processes (p < 0.05). Treatment with CsA + UC-MSC upregulated superoxide dismutase activity compared with CsA + UCB-Treg treatment. Adding UC-MSC or UCB-Treg to CsA markedly enhanced the reconstruction of hematopoiesis in AA mice, with UC-MSC eliciting greater efficiency than UCB-Treg. Accordingly, the addition of these cells could further improve immune abnormalities.

Maillard-type glycated collagen with alginate oligosaccharide suppresses inflammation and oxidative stress by attenuating the expression of LPS receptors Tlr4 and Cd14 in macrophages.

Inflammation and oxidative stress contribute to noncommunicable diseases (NCDs), with macrophages playing pivotal roles. Glycated collagen through Maillard-type glycation holds promise for enhancing anti-inflammatory properties, but its mechanism remains unclear. This study investigates the cellular mechanism and aims to contribute to expanding collagen utilization. Collagen was glycated with alginate oligosaccharide (AO) and glucose (Glc: as a comparative case) at 60 °C and 35% relative humidity for up to 24 h (C-AO and C-Glc, respectively). The anti-inflammatory activities of both C-AO and C-Glc were evaluated using an LPS-stimulated macrophage model. 18 h AO-glycated collagen (C-AO18 h) was found to significantly reduce the production of nitric oxide and proinflammatory cytokines (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). In contrast, C-Glc did not exhibit enhanced anti-inflammatory activity during any of the glycation periods. The enhanced anti-inflammatory activity of C-AO18 h was attributed to its downregulating effect on LPS receptors (toll-like receptor 4, Tlr4; cluster of differentiation 14, Cd14) and myeloid differentiation primary response 88 (Myd88) mRNA expression, with suppression in receptor expression resulting in decreased phagocytic ability of macrophages against E. coli. In addition, compared with intact collagen, C-AO18 h exhibited improved antioxidant activity in the LPS-stimulated macrophage model, as it significantly upregulated superoxide dismutase (SOD) and catalase (CAT) activities while reducing malondialdehyde (MDA) levels. Overall, this study contributes to the development of collagen-based functional foods for mitigating inflammation and oxidative stress in NCDs.

Montmorillonite-based edible coating enhances the postharvest quality of sweetpotato by regulating ROS and membrane lipid metabolism

The quality deterioration of sweetpotatoes easily during postharvest storage owing to their high respiration rate and accumulation of reactive oxygen species (ROS). In this study, an edible coating (MCW) assembled using montmorillonite, chitosan, and whey protein isolate was fabricated to improve the postharvest quality of sweetpotatoes, and the regulatory mechanism of the edible coating treatment on sweetpotato quality has investigated. The results confirmed that edible coating treatment had a positive effect on maintaining the appearance, firmness, colour, and sensory quality of sweetpotatoes, especially in maintaining free water, starch and soluble protein content, inhibiting respiration rate and delaying weight loss of sweetpotatoes stored at 25 °C for 30 d. Meanwhile, this study illuminated the MCW coating regulates ROS metabolism by upregulating superoxide dismutase, ascorbate peroxidase, and glutathione reductase gene expression, resulting in lower O2−. content in postharvest sweetpotato. Furthermore, the relative expression of the genes encoding lipoxygenase, phospholipase C, and phospholipase D was downregulated by the edible coating treatment and contributed to lower enzyme activity, electrolyte leakage and malondialdehyde content, which further reduced the degree of membrane lipid peroxidation and effectively maintained the structure of plasma membrane and then protected the cell integrity of sweetpotato. Collectively, this study provides useful information at the transcriptional level that MCW coating can enhance the post-harvest quality of sweetpotatoes by regulating ROS and membrane lipid metabolism.

Shenshuaifu Granule Attenuates Acute Kidney Injury by Inhibiting Ferroptosis Mediated by p53/SLC7A11/GPX4 Pathway.

Acute kidney injury (AKI) is a common clinical condition resulting in a rapid decline in renal function, and requires improvement in effective preventive measures. Ferroptosis, a novel form of cell death, is closely related to AKI. Shenshuaifu granule (SSF) has been demonstrated to prevent AKI through suppressing inflammation and apoptosis. This study aimed to explore whether SSF can inhibit ferroptosis in AKI. Active ingredients in SSF were detected through HPLC-MS/MS, and their binding abilities with ferroptosis were evaluated by molecular docking. Then, male C57/BL/6J mice were randomly divided into control, cisplatin, and cisplatin+SSF groups. In the latter two groups, mice were intraperitoneally injected with 20 mg/kg of cisplatin. For five consecutive days prior to cisplatin injection, mice in the cisplatin+SSF group were gavaged with 5.2 g/kg of SSF per day.72 h after cisplatin injection, the mice were sacrificed. Serum creatinine (SCr) and blood urea nitrogen (BUN) were measured to evaluate renal function. H&E and PAS staining were used to observe pathological damage of kidney. Cell death was observed by TUNEL staining, and iron accumulation in kidneys of mice was detected by Prussian blue staining. Western blotting, immunohistochemistry, and immunofluorescence were used to investigate the presence of inflammation, oxidative stress, mitochondrial dysfunction, iron deposition, and lipid peroxidation in mouse kidneys. Active ingredients in SSF had strong affinities with ferroptosis. SSF reduced SCr (p<0.01) and BUN (p<0.0001) levels, pathological damage (p<0.0001), dead cells in the tubular epithelium (p<0.0001) and iron deposition (p<0.01) in mice with cisplatin induced AKI. And SSF downregulated macrophage infiltration (p<0.01), the expressions of high mobility group box 1 (HMGB1, p<0.05) and interleukin (IL)-17 (p<0.05), upregulated superoxide dismutase (SOD) 1 and 2 (p<0.01), and catalase (CAT, p<0.05), and alleviated mitochondrial dysfunction (p<0.05). More importantly, SSF regulated iron transport and intracellular iron overload and reduced the expression of ferritin (p<0.05). Moreover, it downregulated the expressions of cyclo-oxygenase-2 (Cox-2, p<0.001), acid CoA ligase 4 (ACSL4, p<0.05), and solute carrier family 7, member 11 (SLC7A11, p<001), upregulated glutathione peroxidase 4 (GPX4, p<0.01) and p53 (p<0.01), and decreased 4-hydroxynonenal (4-HNE) level (p<0.001). SSF attenuates AKI by inhibiting ferroptosis mediated by p53/SLC7A11/GPX4 pathway.

Cinnamon essential oil based on NLRP3 inflammasome and renal uric acid transporters for hyperuricemia

Cinnamon is widely used as a medicinal herb and a culinary spice. The major bioactive component of cinnamon is cinnamon essential oil (CEO). CEO has been reported to have anti-inflammatory and antioxidant effects, but its mechanism of action is not known. In this study, metabolomics was combined with “weighting coefficients” from network pharmacology to identify key pathways and targets, differential metabolites and key metabolic pathways for the therapeutic effects of CEO on Hyperuricemia (HUA), and to precisely investigate the molecular mechanisms of the therapeutic effects of CEO on HUA. Metabolomic analysis revealed that abnormal l-glutamate metabolism and dysregulation of Arachidonic acid (AA) metabolic pathways exacerbated inflammatory responses and oxidative stress, subsequently mediating pathological changes in HUA and exacerbating renal tissue damage. Pharmacodynamic validation showed that CEO alleviated the renal inflammatory response by inhibiting hepatic xanthine oxidase activity, upregulating superoxide dismutase and glutathione peroxidase levels, and downregulating malondialdehyde levels, synergistically inhibiting NLRP3 inflammasome activation, suppressing downstream inflammatory Interleukin-1 beta (IL-1β) and Interleukin-18 (IL-18) secretion, and enhancing antioxidant levels. Additionally, CEO exerted renal protective effects by upregulating the renal transporters OAT1 and ABCG2 and downregulating the GLUT9 and URAT1 levels, resulting in the downregulation of uric acid production and the alleviation of renal tubular lesions. This suggests that CEO could be considered as a potential functional food for kidney damage caused by hyperuricemia.

Electron probe microanalysis and gene expression analysis of melanization caused by summer atrophy virus in the Akoya pearl oyster (Pinctada fucata)

The Akoya pearl oyster, Pinctada fucata, is the major species used for pearl culture in Japan. However, a massive mortality of juvenile and mantle atrophy of adult P. fucata have occurred during summer in Japan's major pearl production areas since 2019, and the symptoms were named “summer atrophy,” where a brown substance was deposited on the inner surface of their shell and mainly at the edge of the mantle. Summer atrophy is caused by a non-enveloped virus with a diameter of <100 nm. This study aimed to reveal whether the deposits are melanin and determine the gene expression in the mantle with the deposition through an infectious experiment. The body fluid of diseased P.fucata containing the causative virus was inoculated into the adductor muscle of three-year-old P. fucata. P. fucata were sampled at 0 (before injection), 1, 3, 6, 10, 14, 21, and 35 days post-injection. First, an electron probe microanalyzer was used to observe the detailed structure and material composition of the deposits of experimentally and spontaneously diseased P. fucata. Protuberances and wrinkled structures differed from a normal inner surface shell. Cluster analysis of these elemental composition ratios revealed that the brown deposits formed a cluster with the melanin standard, a prismatic layer of Mytilus galloprovincialis. Therefore, the brown deposits were considered to be melanin. The gene expression of infected mantles was analyzed by quantitative PCR. RNA was extracted from the mantle and body fluids, and the gene expression of shell matrix protein genes (msi31 and msi60), tyrosinase genes involved in melanin formation (OT47 and pfty1), and superoxide dismutase (SOD), which is an indicator of reactive oxygen species, was analyzed. A general linear model was created using the presence of deposits as an objective variable, with virus gene copy numbers in the body fluid and mantle and expression levels of the above five genes as explanatory variables. Then, an optimal model was selected. As a result, OT47, msi60, and SOD were selected as explanatory variables. The results suggest that virus infection induced the up-regulation of SOD and tyrosinase, inducing the deposits on the inner surface of shells in summer atrophy. Melanization is known in many animals and plays a major role in immunity, particularly in invertebrates. In bivalves, melanization caused by bacterial diseases has been reported, but this is the first report of melanization caused by viral diseases.

Chronic environmentally relevant concentration of copper exposure induces intestinal oxidative stress, inflammation, and microbiota disturbance in freshwater grouper (Acrossocheilus fasciatus)

The influence of chronic environmentally relevant concentration of Cu2+ exposure on fish intestinal health has been rarely studied. In the present study, freshwater grouper (Acrossocheilus fasciatus) was subjected to 0 (control), 0.01 mg/L Cu2+ (Cu0.01), and 0.04 mg/L Cu2+ (Cu0.04) for 30 days. The Cu0.04 group obtained a significantly reduced survival rate, weight gain, and feed intake compared to the control group (P < 0.05). Both levels of Cu2+ exposure induced oxidative stress, evidenced by increased antioxidant enzymes’ activities and malondialdehyde (MDA) contents in the intestine and serum. Based on 16S rDNA analysis, both levels of Cu2+ exposure significantly reduced intestinal microbiota community richness. In the Cu2+ exposure groups, Firmicutes/Bacteroidota ratio, and potentially pathogenic bacteria, such as Proteobacteria, genus Pseudomonas, Citrobacter, Shinella, and Aeromonas were enriched. Meanwhile, the richness of probiotic bacteria, such as Fusobacteriota, Planctomycetota, Cetobacterium, Gemmobacter, and Gemmata were significantly reduced by Cu2+ exposure. Both levels of Cu2+ exposure significantly reduced villus length, lamina propria width, and muscular thickness in the foregut and hindgut, but increased intestinal goblet cell numbers. 0.04 mg/L Cu2+ exposure significantly upregulated superoxide dismutase (sod), pro-inflammation genes nuclear factor kappa b subunit 1 (nfκb1) and interleukin 1 beta (il1β) expression, but downregulated anti-inflammation gene transforming growth factor beta 1 (tgfβ1) expression. In summary, chronic environmentally relevant concentrations of Cu2+ exposure induced intestinal oxidative stress, inflammation, prevalence of pathogen and inhibition of probiotic bacteria, and damage intestinal integrity of freshwater grouper.

Restoration of mitochondrial function by Spirulina polysaccharide via upregulated SOD2 in aging fibroblasts

Reactive oxygen species (ROS), such as superoxide, are crucial factors involved in the stimulation of cellular aging. Mitochondria, which are important organelles responsible for various metabolic processes in cells, produce ROS. These ROS impair mitochondrial function, thereby accelerating aging-related cellular dysfunction. Herein, we demonstrated that the Spirulina polysaccharide complex (SPC) restores mitochondrial function and collagen production by scavenging superoxide via the upregulation of superoxide dismutase 2 (SOD2) in aging fibroblasts. We observed that SOD2 expression was linked to inflammatory pathways; however, SPC did not upregulate the expression of most inflammatory cytokines produced as a result of induction of LPS in aging fibroblasts, indicating that SPC induces SOD2 without activation of inflammatory pathways. Furthermore, SPC stimulated endoplasmic reticulum (ER) protein folding by upregulating ER chaperones expression. Thus, SPC is proposed to be an antiaging material that rejuvenates aging fibroblasts by increasing their antioxidant potential via the upregulation of SOD2.

Mating modifies the expression of crucial oxidative-reductive transcripts in the pig oviductal sperm reservoir: is the female ensuring sperm survival?

Mating induces large changes in the female genital tract, warranting female homeostasis and immune preparation for pregnancy, including the preservation of crucial oxidative status among its pathways. Being highly susceptible to oxidative stress, sperm survival and preserved function depend on the seminal plasma, a protection that is removed during sperm handling but also after mating when spermatozoa enter the oviduct. Therefore, it is pertinent to consider that the female sperm reservoir takes up this protection, providing a suitable environment for sperm viability. These aspects have not been explored despite the increasing strategies in modulating the female status through diet control and nutritional supplementation. To test the hypothesis that mating modifies the expression of crucial oxidative-reductive transcripts across the entire pig female genital tract (cervix to infundibulum) and, particularly in the sperm reservoir at the utero-tubal junction, before ovulation, a period dominated by estrogen stimulation of ovarian as well as of seminal origin. The differential expression of estrogen (ER) and progesterone (PR) receptors and of 59 oxidative-reductive transcripts were studied using a species-specific microarray platform, in specific segments of the peri-ovulatory sow reproductive tract in response to mating. Mating induced changes along the entire tract, with a conspicuous downregulation of both ER and PR and an upregulation of superoxide dismutase 1 (SOD1), glutaredoxin (GLRX3), and peroxiredoxin 1 and 3 (PRDX1, PRDX3), among other NADH Dehydrogenase Ubiquinone Flavoproteins, in the distal uterus segment. These changes perhaps helped prevent oxidative stress in the area adjacent to the sperm reservoir at the utero-tubal junction. Concomitantly, there were a downregulation of catalase (CAT) and NADH dehydrogenase (ubiquinone) oxidoreductases 1 beta subcomplex, subunit 1 (NDUFB1) in the utero-tubal junction alongside an overall downregulation of CAT, SOD1, and PRDX3 in the ampullar and infundibulum segments. Natural mating is an inducer of changes in the expression of female genes commanding antioxidant enzymes relevant for sperm survival during sperm transport, under predominant estrogen influence through the bloodstream and semen. The findings could contribute to the design of new therapeutics for the female to improve oxidative-reductive balance.

Bifidobacterium animalis A12 and Lactobacillus salivarius M18-6 Alleviate Alcohol Injury by keap1-Nrf2 Pathway and Thioredoxin System.

Excessive drinking can significantly damage people's health and well-being. Although some lactic acid bacterial strains have been previously shown to alleviate the symptoms of alcohol injury, the mechanism underlying these effects remains unclear. The aim of this study was to establish an alcohol injury model and examine the protective effect and mechanism of B. animalis A12 and L. salivarius M18-6. The results showed that A12 freeze-dried powder could maintain the survival rate of mice with alcohol injury at 100%. Compared with Alco group, L. salivarius M18-6 dead cell improved the survival rate of mice, attenuated liver steatosis, and significantly down-regulated serum Alanine transaminase (ALT) level; at the same time, it activated keap1-Nrf2 signaling pathway and up-regulated Superoxide dismutase (SOD), it protects mouse liver cells from oxidative stress induced by alcohol injury. In addition, B. animalis A12 can reduce the stress response to short-term alcohol intake and improve the ability of anti-oxidative stress by upregulating the level of isobutyric acid, reducing the level of keap1 protein in the liver of mice and upregulating the expression of thioredoxin genes (Txnrd1, Txnrd3, Txn1). Taken together, the results showed that B. animalis A12 and L. salivarius M18-6 alleviate alcohol injury in mice through keap1-Nrf2 signaling pathway and thioredoxin system.

Melanin from Sepia pharaonis ink alleviates mucosal damage and reduces inflammation to prevent alcohol-induced gastric ulcers

Melanin (MSI) is the primary component of Sepia pharaonis ink. Studies have demonstrated melanin's anti-inflammatory and antioxidant activities in colitis. In the present study, the protective effect of ink melanin against ethanol-induced gastric mucosal damage in mice was investigated. After oral administration of MSI for 12 days, the mice were treated with anhydrous ethanol (0.2 mL) to establish the gastric ulcer model. Histopathological analysis showed that MSI reduced the ulcer area and bleeding symptoms of gastric tissue. MSI exhibited significant antioxidant properties by upregulating superoxide dismutase (SOD), glutathione (GSH), and catalase (CAT) activities and decreasing malondialdehyde (MDA) content. The expression levels of epidermal growth factor (EGF), epidermal growth factor receptor (EGFR), and prostaglandin E−2 (PGE2) significantly decreased during gastric mucosal injury, while MSI significantly reversed the effects. Furthermore, MSI reduced the expression of inflammatory factors tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) and the protein expression of toll-like receptor 4 (TLR4), p38 mitogen-activated protein kinase (p38 MAPK) and extracellular signal-regulated protein kinases 1/2 (ERK1/2). In addition, MSI repressed gastric cell apoptosis by decreasing the expression of Caspase-3. In conclusion, MSI alleviated ethanol-induced gastric ulcer injury by modulating oxidation stress and inflammatory cytokines and maintaining the mucosal barrier, which can be used as therapeutic functional food or nutritional supplement to prevent gastric ulcers. Meanwhile, the mechanism of MSI targeted gastric TLR4/MAPKs pathway deserves further verification.