Oxidative Stress In Mice Research Articles

Allicin treats myocardial infarction in I/R through the promotion of the SHP2 axis to inhibit p-PERK-mediated oxidative stress.

The study attempted to explore how allicin reduces oxidative stress levels by promoting SHP2 expression to inhibit p-PERK in I/R mice. The GEO database and RNA sequencing were used to predict downstream gene. TTC staining was used to visualize the myocardial infarction area. Masson staining was used to assess the level of fibrosis. IF was used to examine the expression of SHP2, CTGF, ROS. RT-PCR analysis was used to quantify the expression of SHP2 mRNA. Western blot was used to detect the protein expression levels of SHP2, p-PERK, MFN1, NLRP3, NOX2, and NOX3. GEO and transcriptomic data revealed low expression of SHP2 in the heart tissues I/R mice. In the I/R mouse model, TTC staining result showed that allicin can reduce the area of myocardial infarction; Masson staining results indicated that allicin can reduce fibrosis; Macrophage transcriptome sequencing found SHP2 is a target gene of allicin; Immunofluorescence showed allicin can increase SHP2; qPCR results showed allicin can raise SHP2 mRNA level; Immunofluorescence indicated that allicin can inhibit ROS in myocardial infarction tissue, but the specific SHP2-KD eliminates changes in ROS. Western blot analysis demonstrated allicin can increase SHP2 protein and reduce the expression of p-PERK, MFN1, NLRP3, NOX2, and NOX3; SHP2-KD eliminates the expression differences in p-PERK, MFN1, NLRP3, NOX2, and NOX3. Allicin can modulate p-PERK activation by enhancing the expression of SHP2, thereby inhibiting myocardial ischemia-reperfusion-induced oxidative stress in mice.

Effects of Tanacetum parthenium on Chromatin Quality, Sperm Parameters and Oxidative Stress in Mice

Effects of Tanacetum parthenium on Chromatin Quality, Sperm Parameters and Oxidative Stress in Mice

Effects of Auricularia auricula-judae (Bull.) Quél. polysaccharide acid hydrolysate on glucose metabolism in diabetic mice under oxidative stress

BackgroundOxidative stress can lead to uncontrolled glucose metabolism and, thus, diabetes. Auricularia auricula-judae (Bull.) Quél. polysaccharides possess biological activities, such as antioxidant and hypoglycemic effects, but their mechanism of their acid hydrolysates on oxidative stress-injured glucose metabolism disorders is unclear. PurposeUsing diabetic mice, we investigated the effect of the acid hydrolysate of polysaccharides from Auricularia auricula-judae (Bull.) Quél. on improving diabetes. Study design and MethodsThe structural information of sample polysaccharides was measured by high performance gel permeation chromatography, nuclear magnetic resolution, and high performance liquid chromatography. The diabetic model was established by intraperitoneal injection of streptozotocin. For eight consecutive weeks, the mice were orally administered sample polysaccharides (100, 200, and 300 mg/kg b.w. per day) for intervention. The improvement effect of the samples on diabetes was explored by detecting the changes in biochemical indicators in mice, and the underlying mechanism was studied by transcriptomic and metabolomic analysis. ResultsThe results showed that acid hydrolysate of Auricularia auricula-judae (Bull.) Quél. polysaccharides consisted mainly of mannose, xylose, glucuronic acid, and glucose; its weight-averaged molecular weight was 6.3842 × 104 Dalton, its number average molecular weight was 2.9594 × 104 Dalton; and the molecule contained α-Glc(1→4)-, β-Glc(1→3)-, and β-Man(1→4)-linked glycosidic bonds. A total of 100 mg/kg b.w. per day sample was the best intervention concentration. After eight weeks of intervention, the sample polysaccharides significantly reduced dynamic blood glucose and serum lipids, enhanced antioxidant enzyme activities, promoted glucagon like peptide-1 and insulin secretion, improved insulin sensitivity and alleviated insulin resistance in diabetic mice. Transcriptomic and metabolomic analyses showed that sample polysaccharides was able to ameliorate disorders of glucose metabolism by modulating gene expression such as glucokinase; and modulate the state of oxidative stress in mice in vivo by regulating the glutathione metabolism pathway. ConclusionAcid hydrolysate of Auricularia auricula-judae (Bull.) Quél. polysaccharides improved glucose metabolism disorders by slowing down the oxidative stress injury in mice, thereby alleviating diabetes. This study provided a basis for determining the underlying mechanism of the antidiabetic effect of Auricularia auricula-judae (Bull.) Quél. polysaccharides, which would significantly improve the deep development and application of these materials in diabetes control.

Short-term inhalation exposure to cigarette smoke induces oxidative stress and inflammation in lungs without systemic oxidative stress in mice.

Smoking is a well-established risk factor for various pathologies, including pulmonary diseases, cardiovascular disorders, and cancers. The toxic effects of cigarette smoke (CS) are mediated through multiple pathways and diverse mechanisms. A key pathogenic factor is oxidative stress, primarily induced by excessive formation of reactive oxygen species. However, it remains unclear whether smoking directly induces systemic oxidative stress or if such stress is a secondary consequence. This study aimed to determine whether short-term inhalation exposure to CS induces oxidative stress in extrapulmonary organs in addition to the lung in a murine model. In the experiment, 3R4F reference cigarettes were used to generate CS, and 8-week-old male BALB/c mice were exposed to CS at a total particulate matter concentration of either 0 or 800µg/L for four consecutive days. CS exposure led to an increase in neutrophils, eosinophils, and total cell counts in bronchoalveolar lavage fluid. It also elevated levels of lactate dehydrogenase and malondialdehyde (MDA), markers indicative of tissue damage and oxidative stress, respectively. Conversely, no significant changes were observed in systemic oxidative stress markers such as total oxidant scavenging capacity, MDA, glutathione (GSH), and the GSH/GSSG ratio in blood samples. In line with these findings, CS exposure elevated NADPH oxidase (NOX)-dependent superoxide generation in the lung but not in other organs like the liver, kidney, heart, aorta, and brain. Collectively, our results indicate that short-term exposure to CS induces inflammation and oxidative stress in the lung without significantly affecting oxidative stress in extrapulmonary organs under the current experimental conditions. NOX may play a role in these pulmonary-specific events.

Modulation of chronic obstructive pulmonary disease progression by antioxidant metabolites from Pediococcus pentosaceus: enhancing gut probiotics abundance and the tryptophan-melatonin pathway.

Chronic obstructive pulmonary disease (COPD), a condition primarily linked to oxidative stress, poses significant health burdens worldwide. Recent evidence has shed light on the association between the dysbiosis of gut microbiota and COPD, and their metabolites have emerged as potential modulators of disease progression through the intricate gut-lung axis. Here, we demonstrate the efficacy of oral administration of the probiotic Pediococcus pentosaceus SMM914 (SMM914) in delaying the progression of COPD by attenuating pulmonary oxidative stress. Specially, SMM914 induces a notable shift in the gut microbiota toward a community structure characterized by an augmented abundance of probiotics producing short-chain fatty acids and antioxidant metabolisms. Concurrently, SMM914 synthesizes L-tryptophanamide, 5-hydroxy-L-tryptophan, and 3-sulfino-L-alanine, thereby enhancing the tryptophan-melatonin pathway and elevating 6-hydroxymelatonin and hypotaurine in the lung environment. This modulation amplifies the secretion of endogenous anti-inflammatory factors, diminishes macrophage polarization toward the M1 phenotype, and ultimately mitigates the oxidative stress in mice with COPD. The demonstrated efficacy of the probiotic intervention, specifically with SMM914, not only highlights the modulation of intestine microbiota but also emphasizes the consequential impact on the intricate interplay between the gastrointestinal system and respiratory health.

Hirsutidin protects against hepatic injury by alcohol-induced oxidative stress in mice

In this research, the influence of hirsutidin on mice with alcoholic liver disease was examined. A total of 30 mice were randomly allocated to five groups (n = 6): Normal control group, Ethanol (EtOH) control group, hirsutidin-10, hirsutidin-20, and hirsutidin-20 per se for 4-week. Furthermore, 1 h after the last dosage of the treatment, 5 mL/kg (i.p.) EtOH (56%) was injected to cause hepatic injury. After 5 h of EtOH administration, blood samples were taken, and then the liver was excised for biochemical analysis. Hirsutidin treatment restored the biochemical changes induced by EtOH: serum levels of liver function tests, lipid profile, blood urea nitrogen, antioxidants levels, malondialdehyde, and cytokines. Hirsutidin supplementation also significantly decreased the histopathological abnormalities in EtOH-induced mice. In the present study, hirsutidin was found to have therapeutic potential for the treatment of alcoholic liver disease. Hirsutidin prevented ethanol-induced biochemical and histopathological alterations in the liver, suggesting its hepatoprotective effect.

Retracted: Osthole Attenuates Bleomycin-Induced Pulmonary Fibrosis by Modulating NADPH Oxidase 4-Derived Oxidative Stress in Mice.

[This retracts the article DOI: 10.1155/2021/3309944.].

Codonopsis Radix Inhibits the Inflammatory Response and Oxidative Stress in Chronic Obstructive Pulmonary Disease Mice through Regulation of the Nrf2/NF-κB Signaling Pathway

Introduction: Chronic obstructive pulmonary disease (COPD) is a nonspecific chronic inflammatory lung disease with no known cure. Codonopsis Radix (CR) has been shown to exhibit anti-inflammatory and antioxidant effects. Therefore, this study aimed to investigate the potential anti-inflammatory effects of different CR varieties on COPD mice. Methods: Sixty male-specified pathogen-free grade C57BL/6J mice were randomly divided into 6 groups, 10 mice in each group. The COPD mice model was induced by cigarette smoke extract combined with lipopolysaccharide, and the mice in each group were given corresponding drugs. Lung function was assessed in all mice. Lung tissues were stained with hematoxylin-eosin, Masson, and periodic acid-Schiff stains, and serum levels of interleukin (IL)-8 and tumor necrosis factor (TNF)-α were detected using an ELISA. Further, serum and lung tissue levels of malondialdehyde (MDA) and superoxide dismutase (SOD) were detected by colorimetric assay. Network pharmacology and molecular docking were used to predict signaling pathways, which were validated by Western blot analysis. Results: Compared with the COPD group, the mice in each dosing group of CR exhibited significant reductions in serum IL-8 and TNF-α levels, serum and lung tissue MDA levels, and pathological lung tissue damage, alongside elevations in lung function and SOD levels (p < 0.01). Western blot analysis also indicated significant downregulation of p-p65/p65 and p-IκB-α/IκB-α protein expression, alongside significant upregulation of Nrf2 protein expression in the lung tissues of mice treated with CR (p < 0.01). Conclusion: In summary, CR effectively enhances lung function, minimizes lung tissue damage, and inhibits inflammation and oxidative stress in mice with COPD. Additionally, these findings suggest that inhibition of the Nrf2/NF-κB axis may be a key mechanism of action of CR in the alleviation of COPD.

499 Effect of exogenous oxytocin on placental oxidative stress in mice before onset of labor

499 Effect of exogenous oxytocin on placental oxidative stress in mice before onset of labor

In vivo comparison of antioxidant properties of fucoidan from Fucus vesiculosus after intragastric administration and external application

Fucoidans are sulfated heteropolysaccharides from brown seaweed, known for anticoagulant, anti- inflammatory, antiviral and other properties. The method of administration and the dosage form of the medicinal substance have a significant impact on the bioavailability of the drug, as well as on its metabolism in the body.The purpose of the work was to evaluate the effect of fucoidan from Fucus vesiculosus on the indicators of the antioxidant system in mice with experimental streptozotocin-induced diabetes when administered intragastrically and externally.To evaluate the antioxidant properties of fucoidan in vivo , diabetes mellitus was developed in mice by intraperitoneal administration of streptozotocin and a 1% solution of nicotinic acid. Fucoidan in two dosage forms was administered for 10 days after the formation of the pathology at a dose of 50 mg/kg in the form of tablets intragastrically and 10 mg per animal in the form of an ointment when applied externally. To assess the antioxidant status of animals, the concentration of thiobarbituric acid-reactive products (TBA-RP) in the blood plasma, the level of reduced glutathione (GSH) and catalase activity (CAT) in the erythrocytes were determined.In mice with streptozotocin-induced diabetes against the background of pathology, the process of lipid peroxidation intensified and the effectiveness of the antioxidant system decreased. Fucoidan from F. vesiculosus suppresses systemic oxidative stress in mice with induced type 2 diabetes mellitus. This is achieved due to the inhibition of excessive generation of pro-oxidants (TBA-RP) and a protective effect on the factors of the antioxidant defense system (catalase activity and glutathione content). To the greatest extent, fucoidan, when administered intragastrically, prevents the formation of pro-oxidants, while when applied externally, it has a protective effect to a greater extent due to the activation of antioxidants.

Lactobacillus reuteri JCM 1112 ameliorates chronic acrylamide-induced glucose metabolism disorder via the bile acid-TGR5-GLP-1 axis and modulates intestinal oxidative stress in mice.

Acrylamide (AA) is a toxic food contaminant that has been reported to cause glucose metabolism disorders (GMD) at high doses. However, it is unclear whether chronic low-dose AA can induce GMD and whether probiotics can alleviate AA-induced GMD. Here, C57BL/6N mice were orally administered with 5 mg per kg bw AA for 10 weeks, followed by another 3 weeks of glucagon-like peptide-1 (GLP-1) analogue (dulaglutide) treatment. Chronic low-dose AA exposure increased the blood glucose level and decreased serum insulin and GLP-1 levels, whereas dulaglutide treatment decreased the blood glucose level and increased the serum insulin level in AA-exposed mice. Then, mice were administered with AA or AA + INT-777 (Takeda G-protein-coupled receptor 5 (TGR5) agonist) for 10 weeks. INT-777 treatment reversed AA-induced downregulation of ileal TGR5 and proglucagon (PG) gene expression and decreased the serum GLP-1 level. These findings indicated that chronic low-dose AA induced GMD via inhibiting the TGR5-GLP-1 axis. Finally, mice were administered with AA for 10 weeks, followed by another 3 weeks of Lactobacillus reuteri JCM 1112 supplementation. L. reuteri supplementation significantly increased serum glucose, insulin and GLP-1 levels, upregulated ileal TGR5 and PG gene expression, and effectively restored the imbalance of bile acid (BA) metabolism in AA-exposed mice, demonstrating that L. reuteri ameliorates chronic AA-induced GMD via the BA-TGR5-GLP-1 axis. In addition, L. reuteri significantly enhanced ileal superoxide dismutase and catalase activities and total antioxidant capacity, thereby preventing chronic AA-induced oxidative stress. Our research provides new insights into the GMD toxicity of chronic low-dose AA and confirms the role of probiotics in alleviating AA-induced GMD.

Protective effect of glycyrrhetinic acid against cantharidin-induced hepatotoxicity through reducing oxidative stress in mice

Protective effect of glycyrrhetinic acid against cantharidin-induced hepatotoxicity through reducing oxidative stress in mice

Lipid-lowering and antioxidant effects of Polygonatum fermented liquor: a study on intestinal microbiota and brain-gut axis in mice.

This study aims to investigate the effects of Polygonatum fermented liquor (PFL) on improving lipid metabolism and oxidative stress in mice by regulating the gut microbiota. Forty SPF-grade male Kunming mice were randomly divided into four groups: normal control group (NC), general liquor group (GC), fresh Polygonatum fermented liquor group (FPC), and nine-steam-nine-bask Polygonatum fermented liquor group (NPC). Each group was administered with sterile water, general liquor, fresh Polygonatum fermented liquor, and nine-steam-nine-bask Polygonatum fermented liquor, respectively, by gavage. The mice's liver, brain tissue, serum, and intestinal contents were collected. The indicators of oxidative stress in the liver, four blood lipid indicators, gamma-aminobutyric acid (GABA), and brain-derived neurotrophic factor (BDNF) levels in the brain tissue were measured, liver hematoxylin and eosin (HE) staining was performed, and the gut microbiota in the small intestine were analyzed using 16S rRNA second-generation sequencing technology. Compared with the NC group, the NPC group showed significantly increased liver glutathione peroxidase (GSH-Px) content in mice (p < 0.05), reduced number of lipid droplets in the liver cells, and increased GABA and BDNF content in the brain tissues. The NPC group regulated lipid metabolism by lowering low-density lipoprotein cholesterol (LDL-C) and increasing high-density lipoprotein cholesterol (HDL-C) content in the mouse serum. Gut microbiota analysis showed significant changes in the gut microbiota of mice in the FPC and NPC groups, with increased richness and species diversity. These two groups increased the abundance of beneficial bacteria such as Lactobacillus, unclassified Muribaculaceae, unclassified Bacilli, and uncultured Bacteroidales bacterium while reducing the abundance of harmful bacteria such as Candidatus Arthromitus, and Staphylococcus, with a particularly significant reduction in Staphylococcus (p < 0.05). It is speculated that the two types of PFL may exert lipid-lowering and antioxidant effects by modulating the abundance of these dominant bacteria. Further studies showed that various environmental factors are closely related to the dominant gut bacteria. Malondialdehyde (MDA) was significantly negatively correlated with Lactobacillus and unclassified Bacilli, superoxide dismutase (SOD) was significantly negatively correlated with Staphylococcus (p < 0.01) and significantly negatively correlated with Candidatus Arthromitus (p < 0.05), and HDL-C was significantly negatively correlated with Staphylococcus and Facklamia (p < 0.05). The two types of PFL chosen in this study may exert lipid-lowering and antioxidant effects by modulating the composition and function of the gut microbiota, providing guidance for the industrial application of Polygonatum.

The Chemoprevention of Arthrospira platensis against Diethyl nitrosamine induced Hepatocellular Carcinoma via Amelioration of Oxidative Stress in Mice

Considering that natural antioxidant products do not have any negative side effects; they are an important component in the treatment and prevention of cancer. The purpose of the research was to explore whether Arthrospira platensis (SP) has hepatoprotective characteristics against hepatocellular carcinoma (HCC) in mice under the experimental conditions. The research was carried out with a group of fifty male Balb/c mice, they were then divided into five unique groups. Following is a list of the groups: (I) Group1: the normal control group, (II) Group 2: Hepatocellular carcinoma (HCC) group that was induced by a single injection of Diethyl nitrosamine (DEN) at a dosage of 100 mg/kg intraperitoneally (I. P). This was followed by injections of carbon tetrachloride (CCl4) twice a week 0.5 mg/kg body weight intraperitonially for a total of 22 weeks, beginning 14 days after the initial injection. (III) Group 3: Oral administration of SP at a dose of 250 mg/kg was given to the HCC group. (IV) Group 4, an oral dosage of SP containing 500 mg/kg was given to the animals, whereas (V) Group 5, an oral dose of 250 mg/kg of SP was given and considered as treatment control. The data revealed that the treatment of spirulina resulted in a significant decrease in the activity of glutamate oxaloacetate transaminase (GOT) also known to be AST, glutamate pyruvate transaminase (GPT) also known to be ALT, gamma-glutamate transaminase, and malondialdehyde (MDA). In addition, there was a notable increase in the total protein level, as well as in the activity of superoxide dismutase (SOD) and catalase (CAT), which were both much higher than normal levels. Spirulina has been shown to exhibit chemoprotective qualities, which may be linked to its antioxidant activity and its capacity to reduce lipid peroxidation has been demonstrated in every single study that has been conducted. In addition to this, it has been shown that spirulina can enhance the levels of pro-inflammatory cytokines, which in turn can significantly reduce inflammation.

Canthaxanthin Attenuates the Vascular Aging or Endothelial Cell Senescence by Inhibiting Inflammation and Oxidative Stress in Mice.

Vascular endothelial dysfunction is an early phenotype of aging-related vascular dysfunction. Delaying vascular aging and preventing cardiovascular disease are major public health problems that urgently need to be solved. Scientists have studied various drugs to prevent the occurrence and progress of cardiovascular disease, but progress has been slow. Here, the antisenescence and anti-endothelial damage of canthaxanthin (CX, which is an active molecule from food) has been studied. This study was performed by adding CX to a model of cell senescence and oxidative damage induced by hydrogen peroxide. Cellular senescence markers (e.g., p16, p21, and p53) and oxidative damage markers (e.g., reactive oxygen species, nitric oxide, malondialdehyde, superoxide dismutase) were evaluated by the enzyme-linked immunosorbent assay, laser scanning confocal microscopy, and Western blotting. We found that CX downregulated the expression level of senescence-associated molecules, and significantly reduced the oxidative damage of vascular endothelial cells. These observations showed that CX effectively alleviated the senescence of vascular endothelial cells. Furthermore, CX treatment reduced the expression levels of interleukin-6 (IL-6), tumor necrosis factor alpha, and IL-1β. Finally, in vivo, CX significantly alleviated vascular senescence. The current study shows that CX has potential application value for treating vascular aging or endothelial cell senescence.

Pseudorabies virus causes splenic injury via inducing oxidative stress and apoptosis related factors in mice

Pseudorabies virus (PRV) is an immunosuppressive virus that causes significant damage to the pig industry. This study aimed to investigate the effects of PRV on oxidative stress and apoptotic related in the spleen of mice to provide basis knowledge for further research on the pathogenesis of PRV in mice model. 36 mice were randomly two groups, the control group which only received 200 μL PBS and infection group which was subcutaneously infected with 200 μL of 1 × 103 TCID50/100 μL PRV, respectively. Spleen tissues in each group were collected for further experiments at 48, 72, and 96 h post-infection (hpi). Pathological observation was performed by hematoxylin and eosin Y staining. Biochemical and Flow cytometry methods were used to determine the reactive oxygen species profile and apoptosis of the spleen post-infection and apoptosis detection. In addition, q-PCR and Western blot were adopted to measure the apoptotic conditions of the spleen infected with PRV. The results indicated that the reactive oxygen species (ROS) level in the PRV infection group was remarkedly increased (p < 0.01) at a time-dependent pattern. Furthermore, the Malondialdehyde levels in the spleen of mice in the infection group increased (p < 0.01) in a time-dependent mode. However, the activity of Catalase, Superoxide dismutase, and glutathione peroxidase and the content of Glutathione in the infection group were decreased with the control group (p < 0.01) at a time-dependent manner. In addition, the ratio of splenocyte apoptosis in the infection group significantly increased (p < 0.01) in a time-dependent manner. In conclusion, PRV infection causes apoptosis of the spleen via oxidative stress in mice.

Mesobiliverdin IXα ameliorate DSS-induced colitis by inhibiting inflammation and oxidative stress in mice

Inflammatory Bowel Diseases (IBDs), including ulcerative colitis and Crohn’s disease, are enduring conditions distinguished by inflammation of the intestines and the presence of oxidative stress. The present work aimed to examine the possible mitigating effects of Mesobiliverdin IXα (MBV), a bioactive tetrapyrrole metabolite, on colitis produced by dextran sodium sulfate (DSS) in mice. The mice were divided into four groups: control, DSS, MBV5, and MBV20. The DSS group was administered DSS to induce colitis, while the MBV5 and MBV20 groups received daily doses of Mesobiliverdin IXα at concentrations of 5 μM and 20 μM, respectively, along with DSS treatment. The control group was given a normal diet without DSS. Our results showed that DSS treatment caused significant weight loss in the mice, whereas MBV administration effectively mitigated this weight loss. Although the body weight did not fully recover to the normal level, MBV treatment led to significant improvements in colon weight, colon length, and the ratio of colon weight to colon length. Histological analysis revealed that MBV alleviated the damage to the colon tissue caused by DSS-induced inflammation. Moreover, MBV significantly reduced myeloperoxidase (MPO) activity, indicating a reduction in neutrophil activation and inflammation. Overall, our findings demonstrate that MBV effectively mitigates inflammation and oxidative stress in DSS-induced colitis in mice. This study highlights the therapeutic potential of MBV as a natural compound derived from microalgae, which warrants further investigation for the treatment of IBDs in humans.

Kushenol C from Sophora flavescens protects against UVB-induced skin damage in mice through suppression of inflammation and oxidative stress

Sophora flavescens has been used in traditional medicine for the treatment of various diseases such as viral hepatitis, fever, cancer, and pain. It is known to contain many bioactive compounds including prenylated flavonoids such as kurarinone, sophoraflavanone G, kuraridine and isoxanthohumol. These flavonoids have been confirmed to have anti-inflammatory, α-glucosidase inhibitory and antioxidant performances. However, the protective activities against UV-induced skin damage of kushenol C from S. flavescens have not yet been elucidated. In this study, we explored the protective effect of kushenol C against the skin damage induced by UVB in mice. Our results showed that kushenol C treatment significantly recovered UVB-induced skin damage, the degradation of collagen, mast cell infiltration, together with epidermal hyperplasia in mice. Furthermore, the treatment of kushenol C remarkably suppressed the generation of pro-inflammatory mediators in the mice irradiated by UVB. More so, treatment with kushenol C suppressed the oxidative stress in mice irradiated by UVB. In conclusion, these results showed that kushenol C from S. flavescens has potentialities to treat skin injury via suppressing skin damage induced by UVB and oxidative stress.

Amelioration of Type 2 Diabetes Using Four Strains of Lactobacillus Probiotics: Effects on Gut Microbiota Reconstitution-Mediated Regulation of Glucose Homeostasis, Inflammation, and Oxidative Stress in Mice.

This study aims to explore the preventive effects and underlying mechanisms of Lactobacillus fermentum CKCC1858 (CKCC1), L. fermentum CKCC1369 (CKCC2), Lactobacillus plantarum CKCC1312 (CKCC3), and Lactobacillus gasseri CKCC1913 (CKCC4) on high-fat diet combined with streptozotocin (HFD/STZ)-stimulated type 2 diabetes (T2D) in mice. Generally, the results indicated that most of the four probiotics reduced weight loss and liver and pancreas damage, significantly (p < 0.05) improved glucose metabolism by regulating glucagon-like peptide-1 (GLP-1), fasting glucose and insulin levels, and increasing expression of glucose transporters. Probiotics improved hyperlipemia, inflammation, and oxidative stress by reducing the secretion of blood lipids and proinflammatory cytokines, increasing antioxidant enzymes. Metagenomic results revealed that probiotics restored gut microbiota via enhancing (reducing) the relative abundance of beneficial bacteria (harmful bacteria) and altered specific metabolic pathways in T2D mice. CKCC1, CKCC3, and CKCC4 showed excellent effects compared to CKCC2. These results indicated that probiotics potentially prevented T2D, which is strain-specific.

Physicochemical, functional, and antioxidant properties of black soldier fly larvae protein.

This study explores the multifaceted attributes of black soldier fly larvae protein (BSFLP), focusing on its physicochemical, functional, and antioxidant properties. BSFLP is characterized by 16 amino acids, with a predominant random coil secondary structure revealed by circular dichroism spectra. Differential scanning calorimetry indicates a substantial thermal denaturation temperature of 97.63°C. The protein exhibits commendable solubility, emulsification, and foaming properties in alkaline and low-salt environments, albeit with reduced water-holding capacity and foam stability under elevated alkaline and high-temperature conditions. In vitro assessments demonstrate that BSFLP displays robust scavenging proficiency against 2,2-diphenyl-1-picrylhydrazyl, 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid), and hydroxyl radicals, with calculated EC50 values of 1.90±0.57, 0.55±0.01, and 1.14±0.02mg/mL, respectively, along with notable reducing capabilities. Results from in vivo antioxidant experiments reveal that BSFLP, administered at doses of 300 and 500mg/kg, significantly enhances the activities of antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) (p<0.05) while simultaneously reducing malondialdehyde levels in both serum and tissues of d-galactose-induced oxidative stress in mice. Moreover, the protein effectively attenuates oxidative damage in liver and hippocampal tissues. These findings underscore the potential utility of BSFLP as a natural antioxidant source, with applications spanning the food, pharmaceutical, and cosmetic industries. PRACTICAL APPLICATION: Black soldier fly larvae protein emerges as an environmentally sustainable reservoir of natural antioxidants, holding significant promise for the food, pharmaceutical, and cosmetic sectors. Its advantageous amino acid composition, robust thermal resilience, and impressive functional attributes position it as a compelling subject for continued investigation and advancement in various applications.