Antioxidant Markers Research Articles

Paeoniflorin regulates RhoA/ROCK1 and Nrf2 pathways in PDLIM1-dependent or independent manners in oxidative stressed melanocytes.

The adhesive properties of vitiligo melanocytes have decreased under oxidative stress., cytoskeleton proteins can control cell adhesion. Paeoniflorin (PF) was proved to resist hydrogen peroxide (H2O2)-induced oxidative stress in melanocytes via nuclear factorE2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. This study was to investigate whether PF exerts anti-oxidative effect through influencing cytoskeleton markers or potential signaling pathway. Human Oxidative Stress Plus array was used to identify the differentially expressed genes between H2O2 + PF group and H2O2 only group, in PIG1 and PIG3V melanocyte cell lines respectively. Western blotting was used to verify the PCR array results and to test the protein expression levels of cytoskeleton markers including Ras homolog family member A (RhoA), Rho-associated kinase 1 (ROCK1) and antioxidative marker Nrf2. Small interfering RNA was used to knock down PDZ and LIM domain 1 (PDLIM1). PF increased the expressions of PDLIM1, RhoA and ROCK1 in H2O2-induced PIG1, in contrast, decreased the expressions of PDLIM1 and ROCK1 in H2O2-induced PIG3V. Knockdown of PDLIM1 increased the expressions of RhoA and Nrf2 in PF-pretreated H2O2-induced PIG1, and ROCK1 and Nrf2 in PF-pretreated H2O2-induced PIG3V. PF regulates RhoA/ROCK1 and Nrf2 pathways in PDLIM1-dependent or independent manners in H2O2-induced melanocytes. In PIG1, PF promotes PDLIM1 to inhibit RhoA/ROCK1 pathway or activates Nrf2/HO-1 pathway, separately. In PIG3V, PF directly downregulates ROCK1 in PDLIM1-independent manner or upregulates Nrf2 dependent of PDLIM1.

Investigating the association between blood oxidative stress markers and dementia in Egyptian elderly women

BackgroundThe predicted increase in the senior population will have a substantial impact on mental health and dementia development, emphasizing the need to study the biochemical components related to the pathogenesis of dementia. Oxidative stress is caused by an imbalance between the production of reactive oxygen species and the antioxidant balance of the body. The brain is particularly vulnerable to oxidative stress because of the relatively low levels of antioxidants in the brain, high levels of polyunsaturated fatty acids, and increased oxygen needs. The increase of reactive oxygen species leads to the accumulation of protein oxidation by-products which has a key role in dementia pathogenesis. The aim of the study is to investigate the link between oxidative stress and dementia in Egyptian older women and its possible effect on dementia severity and types. A case–control study was conducted involving 40 elderly women with dementia, and another 40 cognitively intact controls. All participants were subjected to a comprehensive geriatric evaluation, which included cognitive assessment, depression screening, and functional assessment. Blood levels of malondialdehyde (an oxidative stress marker), glutathione peroxidase enzyme and total antioxidant capacity (an antioxidant markers) were measured.ResultsMalondialdehyde’s blood level was significantly higher in dementia cases (p < 0.001), indicating a higher oxidative stress status in dementia cases. While blood levels of both glutathione peroxidase enzyme and total antioxidant capacity were significantly lower in dementia cases (p < 0.001), indicating a lower antioxidant activity in dementia cases. We found that glutathione peroxidase enzyme at a cutoff point ≤ 122 mu/ml, total antioxidant capacity at a cutoff point ≤ 39.1 mm/l, and malondialdehyde at a cutoff point > 95 nmol/ml had perfect diagnostic value for identifying patients with dementia.ConclusionOxidative stress showed a significant role in the pathogenesis of dementia, with the presence of higher levels of oxidative damage by-products and lower levels of antioxidant status. So, the role of oxidative stress in dementia should not be neglected, and more effort should be directed to prevent unnecessary exposure to oxidative stress in older adults to contribute towards dementia prevention.

Mitigative Effects of l-Arginine and N-Acetyl Cysteine against Cisplatin-Induced Testicular Dysfunction and Toxicity through the Regulation of Antioxidant, Anti-inflammatory, and Antiapoptotic Markers: Role of miR-155 and miR-34c Expression.

Testicular dysfunction is a common adverse effect of cisplatin (CIS) administration as a chemotherapeutic drug. The current study has outlined the role of micro-RNAs (miR-155 and 34c) in CIS-induced testicular dysfunction and evaluated the protective effect of N-acetyl cysteine (NAC) and/or l-arginine (LA). Seven groups of Albino rats were used for this study. The control (C) group received physiological saline; the CIS group was injected CIS (7 mg/kg IP, once) on day 21 of the experiment; the NAC group was administered NAC (150 mg/kg intragastric, for 28 days); and the LA group was injected LA (50 mg/kg IP, for 28 days). NAC+CIS, LA+CIS, and NAC+LA+CIS groups received the above regime. CIS significantly reduced serum testosterone, LH, and FSH concentrations with decline of testicular enzyme activities. CIS caused significant elevation in testicular oxidative-stress biomarkers, inflammation-associated cytokines, and apoptosis markers, along with overexpression of miR-155 and low miR-34c expression. Additionally, marked testicular degenerative changes were observed in the examined histological section; a significant decrease in the expression of PCNA with significant increase in expressions of F4/80 and BAX was confirmed. The administration of NAC or LA upregulated testicular functions and improved histopathological and immunohistochemical changes as well as miRNA expression compared with the CIS-administered group. Rats receiving both NAC and LA showed a more significant ameliorative effect compared with groups receiving NAC or LA alone. In conclusion, NAC or LA showed an ameliorative effect against CIS-induced testicular toxicity and dysfunction through the regulation of antioxidant, anti-inflammatory, and antiapoptotic markers and via modulating miR-155 and miR-34c expression.

The Effects of Dietary Saccharomyces cerevisiae Supplementation on Gut Microbiota Composition and Gut Health in Aged Labrador Retrievers.

The intestinal microbiome changes with age, influencing the host's health and immune status. Saccharomyces cerevisiae (S. cerevisiae) positively affects intestinal function in humans and animals, but its effects on gut health and the microbiota profile in aged dogs have not been thoroughly investigated. Twenty aged Labrador Retrievers were divided into two groups: a control group (CON) and a S. cerevisiae group (SC). The experiment lasted for 42 days, with assessments of their intestinal barrier function, inflammatory factors, antioxidant markers, and fecal microbiome composition. The results showed that dietary S. cerevisiae reduced the levels of TNF-α, IL-6, and IL-1β in the serum (p < 0.05). In the SC group, plasma superoxide dismutase and glutathione peroxidase activities increased, while the level of malondialdehyde significantly decreased (p < 0.05). Additionally, dietary S. cerevisiae lowered the serum zonulin and lipopolysaccharide (LPS) levels (p < 0.05) and inhibited fecal ammonia production (p < 0.05). Furthermore, the microbiota profile showed that dietary S. cerevisiae decreased the abundance of Firmicutes but increased the Chao index, the abundance of Bacteroidetes, and the proportion of Bacteroidetes to Firmicutes (p < 0.05). To conclude, dietary S. cerevisiae can regulate the gut's microbial structure and gut health, which may contribute to the overall health of companion animals as they age.

Pre-clinical studies comparing the anti-inflammatory potential of artemisinic compounds by targeting NFκB/TNF-α/NLRP3 and Nrf2/TRX pathways in Balb/C mice.

Artemisinin, artemether, artesunate, and dihydroartemisinin are renowned for their antimalarial potential. The current study aims to repurpose the above-mentioned artemisinic compounds (ACs) by conducting an intercomparison to evaluate their antiinflammatory potential (AIP). In order to develop potential candidates for the evaluation of AIP of ACs (50 and 100 mg/kg BW), carbon tetrachloride (1ml/kg body weight (BW)) was administered intraperitoneally to BALB/c mice. Alterations in animal behavior were assessed weekly through tail suspension test, force swim test, open field test, Y-maze test, inverted screen analysis, and weight lifting test. Aberrations in hematological, serological, endogenous antioxidants, and oxidative stress marker profiles were assessed in all twelve groups. Histological alterations were read using hematoxylin and eosin staining. Levels of inflammatory markers including nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3), were determined using immunohistochemical analysis (IHCA). Antioxidant markers i.e., nuclear factor erythroid-2-related factor (Nrf-2) and thioredoxin (TRX) were also quantified through IHCA. Comet assay was performed to quantify DNA damage. Oral administration of ACs to mice significantly alleviated the carbon tetrachloride induced inflammation in comparison with silymarin. Reduced levels of several inflammatory markers including nitric oxide, thiobarbituric acid reactive substances, interleukin-1 beta, NF-κB, TNF-α, and NLRP3, underscore the substantial AIP of ACs. IHCA depicted the revitalized percent relative expression of Nrf-2 and TRX in groups treated with ACs. Behavioral analysis revealed that ACs-treated groups significantly (p<0.05) attenuated the memory deficit, anxiety, and depressive-like behavior. Moreover, histopathological, hematological, serological, and endogenous antioxidant profiles indicated substantial AIP of ACs. Findings of comet assay further bolstered the compelling evidence as DNA damage was significantly (p<0.05) curbed down after ACs (100 mg/kg) treatment. All these outcomes implied that ACs exhibited AIP in a dose-dependent manner with maximal AIP imparted by artemisinin (100 mg/kg). This pre-clinical investigation avers the tremendous AIP of ACs targeting key molecular pathways. The current study divulges artemisinin as the most potent antiinflammatory agent among the tested compounds.

P-Coumaric acid pronounced protective effect against potassium bromate-induced hepatic damage in Swiss albino mice.

Potassium bromate (KBrO3) is a common dietary additive, pharmaceutical ingredient, and significant by-product of water disinfection. p-coumaric acid (PCA) is a naturally occurring nutritional polyphenolic molecule with anti-inflammatory and antioxidant activities. The goal of the current investigation was to examine the protective effects of p-coumaric acid against the liver damage caused by KBrO3. The five groups of animals-control, KBrO3 (100 mg/kg bw), treatment with KBrO3 along with Silymarin (100 mg/kg bw), KBrO3, followed by PCA (100 mg/bw, and 200 mg/kg bw) were randomly assigned to the animals. Mice were slaughtered, and blood and liver tissues were taken for assessment of the serum biochemical analysis for markers of liver function (alanine transaminase, aspartate transaminase, alkaline phosphatase, albumin, and protein), lipid markers and antioxidant markers (TBARS), glutathione peroxidase [GSH-Px], glutathione (GSH), and markers of hepatic oxidative stress (CAT), (SOD), as well as histological H&E stain, immunohistochemical stain iNOS, and COX-2 as markers of inflammatory cytokines. PCA protects against acute liver failure by preventing the augmentation of blood biochemical markers and lipid profiles. In mice liver tissues, KBrO3 increases lipid indicators and depletes antioxidants, leading to an increase in JNK, ERK, and p38 phosphorylation. Additionally, PCA inhibited the production of pro-inflammatory cytokines and reduced the histological alterations in KBrO3-induced hepatotoxicity. Notably, PCA effectively mitigated KBrO3-induced hepatic damage by obstructing the TNF-α/NF-kB-mediated inflammatory process signaling system. Additionally, in KBrO3-induced mice, PCA increased the intensities of hepatic glutathione (GSH), SOD, GSH-Px, catalase, and GSH activities. Collectively, we demonstrate the molecular evidence that PCA eliminated cellular inflammatory conditions, mitochondrial oxidative stress, and the TNF-α/NF-κB signaling process, thereby preventing KBrO3-induced hepatocyte damage.

Therapeutic potential of Capparis spinosa in experimental model of acute acetic acid-induced colitis: Anti-inflammatory and antioxidant effects

IntroductionThis study examined the anti-inflammatory and antioxidant properties of Capparis spinosa L. (caper) in order to determine its medicinal potential in the treatment of acute colitis. MethodSixty male rats were divided into six groups. After the experimental period, distal colonic extension was collected for determination of colonic damage, oxidative stress markers, along with antioxidant markers. The impact of altered levels of inflammatory cytokines in colon tissues on the underlying mechanisms examined. ResultsThe results showed that administering different doses of caper led to significant decreases in TNF-α and IL-6 levels when compared to the control colitis group (p < 0.001). Caper treatment effectively lowered elevated oxidative stress factors (MDA, NO, and MPO) compared to the control colitis group (p < 0.001). Caper treatment resulted in a significant increase in antioxidant factors (CAT, SOD, and GSH) compared with the control colitis group (p < 0.001).Significant improvements in tissue repair were observed in caper-treated groups compared to positives and control colitis (p < 0.001). ConclusionThe study highlights caper may be useful in the treatment of acute colitis due to its ameliorative effects on inflammation, oxidative stress, and tissue repair.

Impact of thermal manipulation during embryogenesis on thermotolerance and semen quality of Mandarah roosters exposed to heat stress.

The management of incubation conditions impacts embryonic development, hatchability, and post-hatch performance. This study aimed to examine the effects of thermal manipulation (TM) during embryonic development on roosters' thermotolerance, antioxidant activity, immunity, and semen quality under heat-stress conditions. 1200 fertile eggs were distributed evenly between two groups, each containing three replicates (200 eggs/replicate). The first group (G1) was held in the commercial setter with a consistent temperature of 37.5°C and 55% relative humidity (RH) through the 18-day incubation period, acting as a control, while the second group (G2) experienced these conditions until only the 11th day. The eggs were incubated at 39.5°C with 60% RH for 4 h each day from the 12th to the 18th day. From the 19th to 22nd incubation days, both groups maintained a consistent temperature of 37.2°C with a RH of 70%. Two hundred hatched male chicks per treatment group were moved into a closed-system house. All roosters were exposed to a 6-h daily heat challenge with a temperature of 35°C and a humidity of 70% between their 36th and 40th weeks of age. Roosters of G2 exposed to thermal challenge showed improvements (p ≤ 0.05) in multiple blood biochemical, antioxidant, and immunity markers, including total protein, globulin, aspartate aminotransferase, alanine aminotransferase, triiodothyronine, thyroxine, corticosterone, testosterone, total antioxidant capacity, malondialdehyde, immunoglobulin G, immunoglobulin M, and immunoglobulin A levels. Improved semen quality characteristics, including ejaculate volume, sperm concentration, motility, livability, and quality factor, as well as enhanced thermoregulation in post-hatch cocks, were also achieved (p ≤ 0.05). To boost antioxidant activity, immunity, thermotolerance, and semen parameters in roosters under heat-stress conditions, TM application during egg incubation, specifically at 12-18 days, is recommended.

The interactive effect of seven weeks aerobic exercise training and piperine against paraquat-induced lung damage in male Wistar rats: Investigating role of oxidative and inflammatory indices

We aimed to evaluate the effects of seven weeks of aerobic exercise training and piperine on paraquat-induced lung damage. Forty-eight male Wistar rats (230 g, six-eight weeks old) were randomly divided into six groups (n = 8): sham, paraquat (5 mg/kg three times a week; intraperitoneally), paraquat + piperine (10 mg/kg/day; orally), paraquat + aerobic exercise training, paraquat + piperine + aerobic exercise training; and paraquat + vitamin E (20 mg/kg/day; orally) as a positive control. Rats were sacrificed on day 50, and both lung tissues were isolated to measure oxidative (MDA), anti-oxidative (GSH), inflammatory (TNF-α), anti-inflammatory (IL-10) markers, and histological evaluations (hematoxylin-eosin staining). The results of the present study revealed that paraquat significantly decreased body weight, GSH, GSH/MDA ratio, IL-10, and IL-10/TNF-α ratio while increasing MDA, TNF-α, and histopathological damage in lung tissue (P < 0.01 to 0.001). In contrast, treatment with all four interventions meaningfully diminished oxidative, inflammatory markers, and histopathological damage while propagating body weight, anti-oxidative and anti-inflammatory markers following the paraquat-induced lung damage (P < 0.05 to P < 0.001). Interestingly, piperine and piperine + exercise training possessed stronger protective effects against paraquat-induced lung damage than exercise training alone (P < 0.01 to 0.001). Treatment with piperine, exercise training, piperine + exercise training, and vitamin E significantly ameliorated paraquat-induced lung damage. Interestingly, the piperine and piperine + exercise training had more protective effects than other groups. Therefore, piperine and the combination of piperine and exercise training may be valuable candidates for preventing lung injuries.

Unveiling osteoprotective potential of biologically active naringenin in rats with dexamethasone-induced osteoporosis

ObjectiveTo investigate the protective effects of naringenin (NRG) against dexamethasone (DEX)-induced osteoporosis (OP) in rats. MethodsMolecular docking of NRG was done with AutoDock Vina 1.2.0 software. Forty-eight female Wistar rats were randomly divided into six groups (n = 8 each): normal control (NC), DEX (7 mg/kg, i.m.), NRG-low (NRG-L; 25 mg/kg, i.g.), NRG-medium (NRG-M; 50 mg/kg, i.g.), NRG-high (NRG-H; 100 mg/kg, i.g.), and alendronate (ALN; 0.25 mg/d, i.g.) groups. OP was induced by administering DEX once a week for five weeks in all groups except NC group. Begining in the third week after the initial DEX administration, the rats in NRG-L, NRG-M, NRG-H, and ALN groups received the corresponding treatments daily for three weeks, while NC and DEX groups received no additional treatment. Serum samples were collected at the end of the experiment for biochemical, bone turnover, antioxidant, lipid profile, and inflammatory cytokine analyses. Femur bones underwent physical parameter testing and histopathological examination. ResultsThe molecular docking results illustrated that NRG docked with calcitonin (CT), low-density lipoprotein (LDL), bone morphogenetic protein (BMP), vascular endothelial growth factor (VEGF) receptor, forkhead transcription factors, and osteoprogenitor cells showed good binding energy. In rats administered with 25, 50, and 100 mg/kg NRG, there was a significant enhancement in serum biochemical indices, characterized by a reduction in tartrate-resistant acid phosphatase (TRAP), parathyroid hormone (PTH), and an elevation in osteocalcin (OC) and CT levels (P < 0.05, P < 0.01, and P < 0.001, respectively). Despite no significant changes in thickness, weight, and length (P > 0.05), there was a marked increase in bone mineral density (BMD) (P < 0.01, P < 0.001, and P < 0.001, respectively). Antioxidant enzyme markers showed significant upregulation, with higher glutathione, superoxide dismutase, and catalase, and a concurrent decrease in malondialdehyde (MDA) (P < 0.05, P < 0.01, and P < 0.001, respectively). The lipid profile also improved significantly, with lower cholesterol (CH), triglycerides (TG), and low-density lipoprotein (LDL) levels, and an increase in high-density lipoprotein (HDL) level (P < 0.05, P < 0.01, and P < 0.001, respectively). Inflammatory cytokine levels were reduced, as evidenced by decreases in tumor necrosis factor (TNF), interleukin (IL)-6, and IL-1β (P < 0.05, P < 0.01, and P < 0.001, respectively). Furthermore, histological alterations revealed obvious improvements, and the body weight of rats treated with NRG showed an increase compared with DEX group. ConclusionThese findings imply that NRG exhibited a protective effect against DEX-induced OP in rats as it promotes the bone formation process by increasing the number of bone turnover markers including OC and CT, and restoring of antioxidant status, lipid metabolism, and inflammatory markers.

Evaluating the Level of Some Antioxidants and C-Reactive Activators Protein in a Sample of Iraqi Women with Breast Cancer

One of the key causes of cancer is the detrimental effect of reactive oxygen species on DNA repair mechanisms. The present study aims to describe the function of oxidative stress in boosting breast cancer and to point out the potential defense role of antioxidants and some trace elements. In addition, it is to estimate the concentration of C - C-reactive protein (CRP), a marker of inflammation. Methods: This study was carried out at the Al-Anbar Oncology Center between January and June 2023. Sixty women with breast cancer and forty healthy women were recruited into this study. Serum antioxidant activity, such as superoxide dismutase. (SOD), Catalase (CAT), vitamin D3, vitamin B12, and some essential chemical elements such as zinc (Zn), copper (Cu), iron (Fe), and selenium (Se). CRP concentration was assessed. Results: The results reveal a significant (P&lt;0.05) decrease in serum antioxidant concentrations such as SOD, CAT, vitamin D3, and vitamin B12 concentration in serum blood of women with breast cancer compared to the apparently healthy women group. The results showed a significant increase (p &lt;0.05) in the CRP concentration of the blood serum of women with breast cancer compared to the healthy women group. The results showed a significant decrease (p &lt;0.05) in the concentration of Zn, Cu and Fe in the serum blood of women with breast cancer compared to the healthy women group. Additionally, there was a significant increase (p &lt;0.05) in Se concentration in serum blood in women with breast cancer. The percentage of breast cancer is lower in urban areas than in rural areas. Conclusions Women with breast cancer showed high levels of oxidative stress as evidenced by increased oxidant markers and decreased antioxidant markers.

Oxidative balance score as a useful predictive marker for new-onset type 2 diabetes mellitus in Korean adults aged 60 years or older: The Korean Genome and Epidemiologic Study–Health Examination (KoGES-HEXA) cohort

BackgroundThe oxidative balance score (OBS) is a comprehensive pro- and anti-oxidative marker for assessing the risk of various metabolic diseases and cancers. However, it is not well established whether OBS is related to type 2 diabetes mellitus (T2DM), particularly in elderly populations. Therefore, our objective was to investigate the longitudinal effect of OBS on T2DM in a large cohort of Korean adults aged 60 years and older. MethodsWe assessed the data for 3516 participants aged 60 years and older without diabetes mellitus from the Health Examinees cohort of the Korean Genome and Epidemiology Study. We classified the participants into three groups according to OBS tertiles. We prospectively assessed hazard ratios (HRs) with 95 % confidence intervals (CIs) for new-onset T2DM using multivariable Cox proportional-hazard regression models during the mean 3.5 years following the baseline survey. ResultsA total of 109 participants (3.1 %) developed T2DM during a mean follow-up of 3.5 years. The incidence rates per 1000 person-years were 11.73 for the lowest OBS tertile (T1), 8.19 for the second tertile (T2), and 6.23 for the highest tertile (T3). Adjusting for all confounding factors, compared with the referent T1, the HR (95 % CI) of new-onset T2DM was not significant in T2 (0.71 [0.47–1.07]) but was significant in T3 at (0.47 [0.30–0.75]) (p for trend = 0.002). ConclusionsThe study suggests that a OBS could serve as a valuable predictive marker for new-onset T2DM in older adults. Our study suggests that maintaining an appropriate body weight through healthy lifestyle modification has the potential to lower T2DM incidence in elderly. This implies that the OBS may be a useful tool for assessing the incidence of T2DM even in older individuals.

Immunomodulatory effects of single and combined exposure to ZnO and TiO2 nanoparticles on rainbow trout challenged with Aeromonas salmonicida achromogenes

The increasing release of engineered nanoparticles (ENPs) in aquatic ecosystems stresses the need for stringent investigations of nanoparticle mixture toxicity towards aquatic organisms. Here, the individual and combined immunotoxicity of two of the most consumed ENPs, the ZnO and the TiO2 ones, was investigated on rainbow trout juveniles (Oncorhynchus mykiss). Fish were exposed to environmentally realistic concentrations (21 and 210 µg L−1 for the ZnO and 210 µg L−1 for the TiO2) for 28 days, and then challenged with the pathogenic bacterium, Aeromonas salmonicida achromogenes. Antioxidant and innate immune markers were assessed before and after the bacterial infection. None of the experimental conditions affected the basal activity of the studied innate immune markers and the redox balance. However, following the bacterial infection, the expression of genes coding for pro and anti-inflammatory cytokines (il1β and il10), as well as innate immune compounds (mpo) were significantly reduced in fish exposed to the mixture. Conversely, exposure to ZnO NPs alone seemed to stimulate the immune response by enhancing the expression of the IgM and c3 genes for instance. Overall, our results suggest that even though the tested ENPs at their environmental concentration do not strongly affect basal immune functions, their mixture may alter the development of the immune response when the organism is exposed to a pathogen by interfering with the inflammatory response.

Dietary Fiber-Derived Butyrate Alleviates Piglet Weaning Stress by Modulating the TLR4/MyD88/NF-κB Pathway.

During weaning, piglets are susceptible to intestinal inflammation and impairment in barrier function. Dietary fiber (DF) plays an active role in alleviating weaning stress in piglets. However, the effects of different sources of dietary fiber on the performance of weaned piglets are inconsistent, and the mechanisms through which they affect intestinal health need to be explored. Therefore, in this study, sixty weaned piglets were randomly divided into three treatment groups: basal diet (control, CON), beet pulp (BP), and alfalfa meal (AM) according to the feed formulation for a 28-day trial. The results showed that both AM and BP groups significantly reduced diarrhea rate and serum inflammatory factors (IL-1β and TNF-α) and increased antioxidant markers (T-AOC and SOD), in addition to decreasing serum MDA and ROS concentrations in the AM group. At the same time, piglets in the AM group showed a significant reduction in serum intestinal permeability indices (LPS and DAO) and a substantial increase in serum immunoglobulin levels (IgA, IgG, and IgM) and expression of intestinal barrier-associated genes (Claudin1, Occludin, ZO-1, and MUC1), which resulted in an improved growth performance. Interestingly, the effect of DF on intestinal inflammation and barrier function can be attributed to its modulation of gut microbes. Fiber-degrading bacteria enriched in the AM group (Christensenellaceae_R-7_group, Pediococcus and Weissella) inhibited the production of TLR4- through the promotion of SCFAs (especially butyrate). MyD88-NF-κB signaling pathway activation reduces intestinal inflammation and repairs intestinal barrier function. In conclusion, it may provide some theoretical support and rationale for AM to alleviate weaning stress and improve early intestinal dysfunction, which may have implications for human infants.

Generation of Porcine and Rainbow Trout 3D Intestinal Models and Their Use to Investigate Astaxanthin Effects In Vitro.

Astaxanthin (AST) is a natural compound derived from shellfish, microorganisms, and algae, with several healthy properties. For this reason, it is widely used in the diet of humans and animals, such as pigs, broilers, and fish, where its addition is related to its pigmenting properties. Moreover, AST's ability to reduce free radicals and protect cells from oxidative damage finds application during the weaning period, when piglets are exposed to several stressors. To better elucidate the mechanisms involved, here we generate ad hoc pig and rainbow trout in vitro platforms able to mimic the intestinal mucosa. The morphology is validated through histological and molecular analysis, while functional properties of the newly generated intestinal barriers, both in porcine and rainbow trout models, are demonstrated by measuring trans-epithelial electrical resistance and analyzing permeability with fluorescein isothiocyanate-dextran. Exposure to AST induced a significant upregulation of antioxidative stress markers and a reduction in the transcription of inflammation-related interleukins. Altogether, the present findings demonstrate AST's ability to interact with the molecular pathways controlling oxidative stress and inflammation both in the porcine and rainbow trout species and suggest AST's positive role in prevention and health.

Dietary resveratrol improves the flesh quality of Siberian sturgeon (Acipenser baerii) by enhancing myofiber growth, nutrient accumulation and antioxidant capacity

BackgroundIn aquaculture, sturgeons are generally maintained in the confined spaces, which not only hinders sturgeon movement, but also threatens their flesh quality that seriously concerned by aquaculture industry. As a typical antioxidant, resveratrol can improve the flesh quality of livestock and poultry. However, the mechanism of resveratrol’s effect on the muscle of Siberian sturgeon is still unclear.ResultsIn this study, the dietary resveratrol increased the myofiber diameter, the content of the amino acids, antioxidant capacity markers (CAT, LDH and SOD) levels and the expression levels of mTORC1 and MYH9 in muscle of Siberian sturgeon. Further transcriptome analysis displayed that ROS production-related pathways (“Oxidative phosphorylation” and “Chemical carcinogenes-reactive oxygen species”) were enriched in KEGG analysis, and the expression levels of genes related to the production of ROS (COX4, COX6A, ATPeF1A, etc.) in mitochondria were significantly down-regulated, while the expression levels of genes related to scavenging ROS (SOD1) were up-regulated.ConclusionsIn summary, this study reveals that resveratrol may promote the flesh quality of Siberian sturgeon probably by enhancing myofiber growth, nutritional value and the antioxidant capacity of muscle, which has certain reference significance for the development of a new type of feed for Siberian sturgeon.

Reused vegetable oil (rvo) caused brain lipid peroxidation and a decrease in antioxidant markers in normal albino rats

Objective: Repeated use of vegetable cooking oils can lead to the oxidative breakdown of fats and oils, thereby releasing free radicals. This study investigated the impact of reused vegetable oil from fast food vendors in Abakaliki Metropolis on brain lipid peroxidation and antioxidant markers in normal albino rats. Methodology: We formed five (5) experimental groups (A-E) from a total of thirty-five (35) rats, each containing seven (7) albino Wistar rats. We collected the brain samples after 42 days of treatment for various laboratory analyses. Results: The amounts of catalase, superoxide dismutase (SOD), and reduced glutathione (GSH) were all significantly higher in rats that were given fresh vegetable oil (FVO) compared to rats that were given used vegetable oil (RVO). However, animals that had RVO had significantly greater levels of nitric oxide (NO) and malondialdehyde (MDA). In comparison to the control group, the albino rats that got RVO and FVO eventually had a noticeably larger body weight. Conclusion: The results suggest that reusing vegetable cooking oil can have a neurotoxic effect on the brain, and it is advisable to avoid it. According to the study's findings, consumption of reused vegetable oil could be harmful to the brain.

Anti-Vasculogenic, Antioxidant, and Anti-Inflammatory Activities of Sulfated Polysaccharide Derived from Codium tomentosum: Pharmacokinetic Assay.

The purpose of this paper was to investigate the anti-inflammatory and anti-angiogenic activities of sulfated polysaccharide from C. tomentosum (PCT) using carrageenan (CARR)-induced paw edema in a rat model and anti-vasculogenic activity on a chorioallantoic membrane assay (CAM) model. Based on in vitro tests of anti-radical, total antioxidant, and reducing power activities, PCT presents a real interest via its antioxidant activity and ability to scavenge radical species. The in vivo pharmacological tests suggest that PCT possesses anti-inflammatory action by reducing paw edema and leukocyte migration, maintaining the redox equilibrium, and stabilizing the cellular level of several pro-/antioxidant system markers. It could significantly decrease the malondialdehyde levels and increase superoxide dismutase, glutathione peroxidase, and glutathione activities in local paw edema and erythrocytes during the acute inflammatory reaction of CARR. PCT pretreatment was effective against DNA alterations in the blood lymphocytes of inflamed rats and reduced the hematological alteration by restoring blood parameters to normal levels. The anti-angiogenic activity results revealed that CAM neovascularization, defined as the formation of new vessel numbers and branching patterns, was decreased by PCT in a dose-dependent manner, which supported the in silico bioavailability and pharmacokinetic findings. These results indicated the therapeutic effects of polysaccharides from C. tomentosum and their possible use as anti-proliferative molecules based on their antioxidant, anti-inflammatory, and anti-angiogenic activities.

Assessing the Impacts of Different Levels of Nano-Selenium on Growth Performance, Serum Metabolites, and Gene Expression in Heat-Stressed Growing Quails.

Nano-minerals are employed to enhance mineral bioavailability thus promoting the growth and well-being of animals. In recent times, nano-selenium (nano-Se) has garnered significant attention within the scientific community owing to its potential advantages in the context of poultry. This study was conducted to explore the impact of using variable levels of nano-Se on the growth performance, carcass characteristics, serum constituents, and gene expression in growing Japanese quails under both thermoneutral and heat stress conditions. A randomized experimental design was used in a 2 × 3 factorial, with 2 environmental conditions (thermoneutral and heat stress) and 3 nano-Se levels (0, 0.2, and 0.5 mg/kg of diet. The findings revealed that heat stress negatively affected the growth and feed utilization of quails; indicated by the poor BWG and FCR. Additionally, oxidative stress was aggravated under heat stress condition; indicated by increased lipids peroxidation and decreased antioxidant enzymes activities. The addition of nano-Se, especially at the level of 0.2 mg/kg of diet, significantly improved the performance of heat stressed quails and restored blood oxidative status. The expression profile of inflammatory and antioxidant markers was modulated by heat stress and/or 0.2 and 0.5 nano-Se in conjunction with environmental temperature in quail groups. In comparison to the control group, the heat stress-exposed quails' expression profiles of IL-2, IL-4, IL-6, and IL-8 showed a notable up-regulation. Significantly lower levels of the genes for IL-2, IL-4, IL-6, and IL-8 and higher levels of the genes for SOD and GPX as compared to the heat stress group demonstrated the ameliorative impact of 0.2 nano-Se. The expression profiles of IL-2, IL-4, IL-6, and IL-8 are dramatically elevated in quails exposed to 0.5 nano-Se when compared to the control group. SOD and GPX markers, on the other hand, were markedly down-regulated. It was concluded that nano-Se by low level in heat stressed growing quails provides the greatest performance and its supplementation can be considered as a protective management practice in Japanese quail diets to reduce the negative impact of heat stress.

Vincamine alleviates intrahepatic cholestasis in rats through modulation of NF-kB/PDGF/klf6/PPARγ and PI3K/Akt pathways

The defect in the hepatobiliary transport system results in an impairment of bile flow, leading to accumulation of toxic compounds with subsequent liver disorders. Vincamine, a plant indole alkaloid that is utilized as a dietary supplement, has been known for its promising pharmacological activities. For the first time, the present study was planned to estimate, at the molecular level, the potentiality of vincamine against alfa-naphthyl isothiocyanate (ANIT)-induced hepatic cholestasis. Liver function tests were analyzed. Hepatic activity of SOD and levels of GSH and MDA were assessed. Hepatic contents of bax, bcl2, NF-kB, PPARγ, catalase, heme-oxygenase-1, NTCP, and BSEP were evaluated using ELISA. mRNA levels of NF-kB, IL-1β, IL-6, TNFα, PDGF, klf6, PPARγ, and P53 were examined using qRT-PCR. PI3K, Akt and cleaved caspase-3 proteins were assessed using western blotting. Histopathological analyses were performed using hematoxylin & eosin staining. ANIT-induced hepatic cholestasis elevated liver function tests, including AST, ALT, GGT, ALP, and total bilirubin. ANIT reduced the protein expression of NTCP and BSEP hepatic transporters. It induced the expression of the inflammatory genes, TNFα, IL-6, IL-1β, and PDGF, and the expression of NF-kB at the genetic and protein level and suppressed the anti-inflammatory genes, klf6 and PPARγ. Also, antioxidant markers were reduced during ANIT induction such as GSH, SOD, catalase, heme-oxygenase-1 and PI3K/Akt pathway, while MDA levels were elevated. Furthermore, the expression of P53 gene, bax and cleaved caspase 3 proteins were activated, while bcl2 was inhibited. Also, the histopathological analysis showed degeneration of hepatocytes and inflammatory cellular infiltrates. However, vincamine treatment modulated all these markers. It improved liver function tests. It inhibited the expression of NF-kB, TNFα, IL-6, IL-1β and PDGF and activated the expression of klf6 and PPARγ. Furthermore, vincamine reduced MDA levels and induced GSH, SOD, catalase, heme-oxygenase-1 and PI3K/Akt pathway. Additionally, it inhibited expression of P53 gene, bax and cleaved caspase 3 proteins. More interestingly, vincamine showed better outcomes on the hepatic histopathological analysis and improved the alterations induced by ANIT. Vincamine alleviated hepatic dysfunction during ANIT-induced intrahepatic cholestasis through its anti-inflammatory and antioxidant efficacies by the modulation of NF-kB/PDGF/klf6/PPARγ and PI3K/Akt pathways.