Total Superoxide Dismutase Levels Research Articles

Effect of olive leaf (Olea europaea L.) extract addition to broiler diets on the growth performance, breast meat quality, antioxidant capacity and caecal bacterial populations

This study aims to evaluate the effect of olive leaf extract (OLE) on growth performance, breast meat quality, antioxidant capacity and caecal microbiota regulation. OLE containing 51.5% oleuropein, 25.6% polyphenols and 6.2% flavonoids, was designed to different supplement levels ranging from 0.1% OLE (OLE0.1) to 0.5% OLE (OLE0.5) into a basal diet, separately. The whole feeding period lasts for 35 days after 7-day hatching from the egg. 720 1-day-age healthy Arbour Acres male broilers were thus divided into five experimental groups and one control group, consist of 20 broilers per group for six parallel experiments in triplicate. The results showed that the levels of average daily feed intake (ADFI) and average daily weight gain (ADG) of the broilers were decreased (p < 0.05) after the addition of 0.3% OLE. Moreover, the breast meat shear force was decreased by 34.4% (p < 0.05). The glutathione (GSH) levels in the meat were increased by 76.64% (p < 0.05); the levels of total superoxide dismutase (T-SOD) and glutathione peroxidase (GSH-Px) were increased by 50.4% and 120%, respectively. And the malondialdehyde (MDA) levels in the meat were reduced by 34.2% (p < 0.05). Additionally, a decreased intensity of Escherichia coli (p < 0.05) and an increased intensity of Lactobacillus and Bifidobacterium (p < 0.05) were observed. Overall, supplementing 0.3% OLE into daily diet enables enhancing breast meat antioxidation, amplifying the abundance of Lactobacillus and Bifidobacterium as well as diminishing the abundance of E. coli in the caecum. HIGHLIGHTS OLE contains 51.5% oleuropein, 25.6% of TP and 6.2% TF levels. OLE addition at 0.3% lowers shear force and raises the GSH’s level of the meat. OLE causes a decrease in E. coli and an increase in Lactobacillus and Bifidobacterium.

Mechanism of erythropoietin-induced M2 microglia polarization via Akt / Mtor / P70S6k signaling pathway in the treatment of brain injury in premature mice and its effect on biofilm

ABSTRACT We investigated the mechanism of erythropoietin (EPO) in brain injury in premature mice based on Akt/mTOR/p70S6K signaling pathway. The brain injury model group of premature mice was obtained by intraperitoneal injection of lipopolysaccharide during pregnancy. Normal mice were taken as the control group. The model mice were divided into low-dose EPO (1,000 IU/kg, L-EPO), medium-dose EPO (2,500 IU/kg, M-EPO), and high-dose EPO groups (5,000 IU/kg, H-EPO) by intraperitoneal injection. The levels of malondialdehyde (MDA) and total superoxide dismutase (T-SOD) were detected. TUNEL staining and Western blotting were used to detect the differences in neuronal apoptosis index (AI), microglial polarization marker protein, and Akt/mTOR/p70S6K-related protein expression levels in each group. Compared with the control group, the protein levels of AI, MDA, Bax, and iNOS in the model, L-EPO, and M-EPO groups were significantly increased, while the T-SOD level and Bcl-2, ARG1, p-Akt, p-mTOR, and p-70S6K protein levels were significantly decreased (P < 0.05). Compared with the model group, AI, MAD levels and Bax, iNOS protein expression levels in L-EPO, M-EPO, and H-EPO groups were significantly decreased, while T-SOD level and Bcl-2, ARG1, p-Akt, p-mTOR, and p-70S6K protein levels were significantly increased. The changes were dose-dependent. In summary, EPO can activate microglia transformation from M1 to M2 through Akt/mTOR/p70S6K signaling pathway.

Environmental carbon tetrachloride exposure disrupts the liver structure and metabolic detoxification function in mice via p38MAPK/NF-κB/NLRP3 pathway

ABSTRACT We investigated the effects of carbon tetrachloride (CCl4) exposure on liver detoxification. We confirmed that 0.2%-0.8% CCl4 decreased the liver carboxylesterase (CarE), lactate dehydrogenase (LDH) activity and total protein (TP) levels, while 0.2% and 0.8% CCl4 increased the liver acetylcholine esterase (AChE) activity (P< 0.05). It was observed0.4%-0.8% CCl4 increased serum glutathione S-transferase (GST) and catalase (CAT) activity, 0.1%-0.8% CCl4 increased the level of malondialdehyde (MDA), and 0.2% CCl4 increased the level of total superoxide dismutase (T-SOD). The expression of nod-like receptor protein 3 (NLRP3), interleukin-1β (IL-1β), and tumour necrosis factor-α (TNF-α) were significantly elevated in 0.2%-0.8% CCl4 exposure (P< 0.05). The expression of p38MAPK, gasdermin D (GSDMD), and nuclear factor kappa-B kinase (IKK) was decreased in 0.1%-0.8% CCl4 exposure, while the apoptosis was not statistically different in all groups. This indicates that 0.1% CCl4 exposure could damage the liver structure and detoxification function via p38MAPK/NF-κB/NLRP3 pathway.

Preliminary exploration of detoxification mechanism of processing methods on cardiotoxicity induced by radix Tripterygium wilfordii in mice via Nrf2/HO-1 pathway

This study aims to investigate the detoxification effects of different processing methods on the cardiotoxicity induced by radix Tripterygium wilfordii, and preliminarily explore the detoxification mechanism via the nuclear factor E2-related factor 2(Nrf2)/heme oxygenase 1(HO-1) pathway. The raw and processed products [stir-fried product, product stir-fried with Lysimachiae Herba(JQC), product stir-fried with Phaseoli Radiati Semen(LD), product stir-fried with Paeoniae Radix Alba(BS), product stir-fried with Glycyrrhizae Radix et Rhizoma(GC), and product stir-fried with vinegar(CZ)] of radix T. wilfordii were administrated to mice by gavage at a dose of 2 g·kg~(-1)(based on crude drugs) for 28 days. Twenty-four hours after the last administration, we measured the serum biochemical indexes of mice to evaluate the detoxification effect. Furthermore, we determined the expression of key proteins of Nrf2/HO-1 pathway in mouse heart tissue by Western blot and some oxidation/antioxidation-related indexes by corresponding kits to explore the detoxification mechanism. The administration of the raw product elevated the levels of serum creatine kinase, lactate dehydrogenase, and malondialdehyde, a product of cardiac lipid peroxidation(P&lt;0.01), down-regulated the protein levels of Nrf2 and HO-1(P&lt;0.01), and reduced the levels of total superoxide dismutase, glutathione, glutathione peroxidase, and glutathione S-transferase(P&lt;0.01). However, after the administration of the products stir-fried with JQC, LD, BS, GC, and CZ, the abnormalities of the above indexes induced by the raw product were recovered(P&lt;0.05 or P&lt;0.01). In particular, the product stir-fried with JQC showed the best performance. Taken all together, the cardiotoxicity induced by radix T. wilfordii could be attenuated by stir-frying with JQC, LD, BS, GC, and CZ, and the stir-frying with JQC showed the best detoxification effect. The mechanism might be associated with the cardiac antioxidant defense and oxidative damage mitigation mediated by the up-regulated Nrf2.

Evaluation of the efficacy of a novel Vibrio vulnificus vaccine based on antibacterial peptide inactivation in turbot, Scophthalmus maximus

Tongue sole tissue factor pathway inhibitor 2 (TFPI-2) C-terminus derived peptide, TC38, has previously been shown to kill Vibrio vulnificus cells without lysing the cell membrane; thus, the remaining bacterial shell has potential application as an inactivated vaccine. Therefore, this study aimed to evaluate the immune response induced by the novel V. vulnificus vaccine. The protective potential of TC38-killed V. vulnificus cells (TKC) was examined in a turbot model. Fish were intramuscularly vaccinated with TKC or FKC (formalin-killed V. vulnificus cells) and challenged with a lethal-dose of V. vulnificus. The results showed that compared with FKC, TKC was effective in protecting fish against V. vulnificus infection, with relative percent of survival (RPS) rates of 53.29% and 63.64%, respectively. The immunological analysis revealed that compared with the FKC and control groups, the TKC group exhibited: 1) significantly higher respiratory burst ability and bactericidal activity of macrophages at 7 d post-vaccination; 2) increased alkaline phosphatase, acid phosphatase, lysozyme, and total superoxide dismutase levels post-vaccination; 3) higher serum agglutinating antibody titer with corresponding higher serum bactericidal ability, and a more potent serum agglutination effect, as well as an increased IgM expression level; 4) higher expression of immune relevant genes, which were involved in both innate and adaptive immunity. Taken together, this is the first study to develop a novel V. vulnificus inactivated vaccine based on AMP inactivation, and TKC is an effective vaccine against V. vulnificus infection for aquaculture.

Protective effect of oleanolic acid on L02 hepatocyte injury induced by HgCl_2

To investigate the protective effect of oleanolic acid(OA) on HgCl_2 induced liver injury. L02 cells were divided into four groups according to different treatment, control group(Con), oleanolic acid group(OA, 10 μmol/L), HgCl_2 group(HgCl_2, 40 μmol/L) and oleanolic acid + HgCl_2 group(OA + HgCl_2). Cells of control group were given serum-free medium, cells of OA group were pretreated with OA solution for 8 hours, cells of HgCl_2 group were exposed to HgCl_2 solution for 6 hours, cells of OA + HgCl_2 group were pretreated with OA solution for 8 hours, and then exposed to HgCl_2 solution for 6 hours. MTT assay was used to detect cell viability. Laser confocal scanning was used to detect JC-1 probe fluorescence intensity to determine mitochondrial membrane potential. DCFH-DA fluorescence probe combined with flow cytometry was used to detect reactive oxygen species(ROS) level. Annexin V/PI double staining method combined with flow cytometry was used to determine cell apoptosis rate. Catalase(CAT), total superoxide dismutase(T-SOD), glutathione(GSH), malondialdehyde(MDA), Caspase 3 and Caspase 9 kits combined with enzyme labeled instrument were used to determine their activity or content respectively. Compared with the control group, 40 μmol/L HgCl_2 could significantly reduce cell viability, the level was 0.52±0.03(P&lt;0.05), OA pretreatment could significantly inhibit the decrease of cell viability induced by HgCl_2, the level was 0.86±0.05(P&lt;0.05). The result of mitochondrial membrane potential detection showed that cell exposed to 40 μmol/L HgCl_2 significantly reduced the intensity of red fluorescence, and the ratio of red to green fluorescence was 0.23±0.02(P&lt;0.05). OA pretreatment significantly increased red fluorescence, and the ratio of red fluorescence to green fluorescence was 1.32±0.08, which was significantly higher than that of HgCl_2(P&lt;0.05). After exposure to 40 μmol/L HgCl_2, the relative fluorescence intensity of ROS was 1.21±0.07, the apoptosis rate was about 8%, the activity levels of Casepase 3 and Casepase 9 were 3.11±0.20 and 2.94±0.17, respectively, which were all significantly higher than those in the control group(P&lt;0.05). OA pretreatment could significantly alleviate the changes of the above indexes, and the difference was statistically significant compared with HgCl_2 group(P&lt;0.05). The level of T-SOD in HgCl_2 group was(7.68±0.39)U/mL, which was significantly lower than that in control group(P&lt;0.05). Compared to the control group, the level of MDA was significantly increased to(4.99±0.26)nmol/mg(P&lt;0.05). OA pretreatment significantly increased level of T-SOD and decreased the level of MDA, the levels were(13.97±0.71)U/mL and(3.01±0.17)nmol/mg, respectively(P&lt;0.05). A certain concentration of HgCl_2 can induce hepatocyte damage. OA pretreatment may reduce cell damage by improving oxidative stress.

Plasma metabolites associated with physiological and biochemical indexes indicate the effect of caging stress on mallard ducks (Anas platyrhynchos).

ObjectiveCage rearing has critical implications for the laying duck industry because it is convenient for feeding and management. However, caging stress is a type of chronic stress that induces maladaptation. Environmental stress responses have been extensively studied, but no detailed information is available about the comprehensive changes in plasma metabolites at different stages of caging stress in ducks. We designed this experiment to analyze the effects of caging stress on performance parameters and oxidative stress indexes in ducks.MethodsLiquid chromatography tandem mass spectrometry (LC/MS-MS) was used to determine the changes in metabolites in duck plasma at 5 (CR5), 10 (CR10), and 15 (CR15) days after cage rearing and traditional breeding (TB). The associated pathways of differentially altered metabolites were analyzed using Kyoto encyclopedia of genes and genomes (KEGG) database.ResultsThe results of this study indicate that caging stress decreased performance parameters, and the plasma total superoxide dismutase levels were increased in the CR10 group compared with the other groups. In addition, 1,431 metabolites were detected. Compared with the TB group, 134, 381, and 190 differentially produced metabolites were identified in the CR5, CR10, and CR15 groups, respectively. The results of principal component analysis (PCA) show that the selected components sufficiently distinguish the TB group and CR10 group. KEGG analysis results revealed that the differentially altered metabolites in duck plasma from the CR5 and TB groups were mainly associated with ovarian steroidogenesis, biosynthesis of unsaturated fatty acids, and phenylalanine metabolism.ConclusionIn this study, the production performance, blood indexes, number of metabolites and PCA were compared to determine effect of the caging stress stage on ducks. We inferred from the experimental results that caging-stressed ducks were in the sensitive phase in the first 5 days after caging, caging for approximately 10 days was an important transition phase, and then the duck continually adapted.

Transcriptome analysis reveals the hepatoprotective mechanism of soybean meal peptides against alcohol-induced acute liver injury mice

This study aimed was to explore the hepatoprotective potential of soybean meal peptides (SPs) against alcohol-induced liver injury and investigate the underlying mechanisms through transcriptome analysis. The chemical antioxidant analysis of SPs exhibited potent ABTS radical scavenging capacity (11.94 ± 0.41 mg TE/100 mg peptide), ferric reducing antioxidant power (6.42 ± 0.32 mmol Fe2+/100 mg peptide), and oxygen radical absorption capacity (14.78 ± 0.01 mg TE/100 mg peptide). Moreover, SPs increased cell viability and reduced intracellular reactive oxygen species levels in Caco-2 cells by H2O2-induced, and without cytotoxicity. In the mice model, preintervention with SPs reduced the levels of aspartate transaminase/alanine transaminase, total cholesterol, triglyceride and malondialdehyde by alcohol-induced, meanwhile, increased the levels of total superoxide dismutase, glutathione and catalase by alcohol-induced. Histological analysis showed that SPs alleviated the liver injury by alcohol-induced and no toxic effects on the kidneys. According to transcriptome analysis, 1737 genes were significantly differentially expressed (1076 up-regulated and 661 down-regulated) after SPs pretreatment. The main functions of these genes were related to inflammation, lipid metabolism and oxidation. The findings from the present study suggested that SPs produced positive hepatoprotection and showed potential to be used as a dietary supplement or an ingredient of functional food.

Nicotinamide Mononucleotide Combined With Lactobacillus fermentum TKSN041 Reduces the Photoaging Damage in Murine Skin by Activating AMPK Signaling Pathway.

Long-term exposure to UVB (280–320 nm) can cause oxidative skin damage, inflammatory injury, and skin cancer. Research on nicotinamide mononucleotide (NMN) and lactic acid bacteria (LAB) with regard to antioxidation, anti-inflammation, and prevention of other age-related diseases has received increasing attention. In the present study, the in vitro antioxidant analysis showed that NMN combined with Lactobacillus fermentum TKSN041 (L. fermentum TKSN041) has a high scavenging ability on hydroxyl (OH), 2, 2′-azino-bis (3-ethylbenzthiazoline-6-sulphonic acid) diammonium salt (ABTS) and 1, 1-diphenyl-2-picrylhydrazyl (DPPH), and it also possess a good total antioxidant capacity. The animal experimental results show that NMN combined with LAB maintained normal liver morphology of mice and reduced pathological damage to murine skin. NMN combined with LAB significantly increased the serum levels of total superoxide dismutase (T-SOD), catalase (CAT), and interleukin (IL)-10, but reduced the levels of malondialdehyde, advanced glycation end products, tumor necrosis factor (TNF)-α, and IL-6. NMN combined with LAB increased T-SOD, CAT, IL-10, Na+-K+-ATPase, and NAD+ levels in the skin, but reduced TNF-α level in the skin. NMN combined with LAB increased the mRNA expression levels of SOD1, CAT, glutathione (GSH), inhibitor of NF-κB (IκB-α), IL-10, AMP-activated protein kinase (AMPK), adaptor protein, phosphotyros ineinteraction, PH domain and leucine zipper containing 1 (APPL1), peroxisome proliferator-activated receptor γ co-activator-1α (PGC-1α), and forkhead transcription factor O (FOXO) in the skin and liver, but decreased the mRNA expression levels of nuclear factor (NF)-κBp65, TNF-α, IL-6, and rapamycin target protein (mTOR). NMN combined with LAB increased the protein expression levels of AMPK, IκB-α, SOD1, and CAT in the skin tissues and reduced protein expression of NF-κBp65. NMN combined with L. fermentum TKSN041 improved murine skin damage caused by UVB irradiation, and the protective mechanism may be related to activation of the AMPK signaling pathway. The results of this study are expected to provide a reference for preventing and the treating skin photoaging.

Dose-Effect of Zearalenone on the Localization and Expression of Growth Hormone, Growth Hormone Receptor, and Heat Shock Protein 70 in the Ovaries of Post-weaning Gilts.

Zearalenone (ZEA) has an estrogen-like effect, which can injure the reproductive system of animals, causing infertility, and abortion in sows. However, the underlying mechanisms are still not clear. The objective of this study was to assess the effects of ZEA on the localization and expression of growth hormone (GH), growth hormone receptor (GHR), and heat shock protein 70 (Hsp70) in the ovaries of post-weaning gilts. Forty healthy post-weaning gilts were randomly provided one of four diets: normal basal diet supplemented with 0 (control), 0.5 (ZEA0.5), 1.0 (ZEA1.0), and 1.5 (ZEA1.5) mg ZEA/kg. Gilts were housed and fed individually for 35 days; the ovaries were collected after euthanasia for antioxidant index, relative mRNA and protein expression, and immunohistochemical analyses of GH, GHR, and Hsp70. The results revealed that the glutathione peroxidase and total superoxide dismutase levels decreased (p < 0.05), whereas the malondialdehyde level increased (p < 0.05) with increasing ZEA content. The localization pattern of GH, GHR, and Hsp70 in ZEA-treated gilts was the same as that in the control; however, the localization of yellow and brown immunoreactive substances of GH, GHR, and Hsp70 was stronger in the ZEA groups than in the control. The relative mRNA and protein expression of GHR and Hsp70 was the highest in the ZEA1.0 group (p < 0.05), whereas that of GH was the highest in the ZEA0.5 group (p < 0.05). The mRNA and protein expression of GH was lower in the ZEA1.5 group than in the control (p < 0.05). Hsp70 results showed adverse responses to increasing ZEA levels in gilt ovaries, suggesting that Hsp70 played an important role in alleviating ZEA-induced oxidative stress.

Anti-obesity effect of Liupao tea extract by modulating lipid metabolism and oxidative stress in high-fat-diet-induced obese mice.

Liupao tea (LPT) is traditional dark Chinese tea. The effect of LPT extract on high-fat-diet-induced obese mice was investigated systematically. The results showed that LPT extract could reduce body weight and significantly alleviate liver damage and fat accumulation. LPT could also decrease the levels of alanine aminotransferase (ALT), aspartate transaminase (AST), alkaline phosphatase (AKP), total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) and increase the level of high-density lipoprotein cholesterol (HDL-C) in the liver. It also decreased the serum levels of inflammatory cytokines, including tumor necrosis factor alpha (TNF-α), interferon gamma (IFN-γ), interleukin (IL)-1β, and IL-6 and increased the serum levels of anti-inflammatory cytokines, including IL-10 and IL-4. Moreover, LPT improved the levels of total superoxide dismutase (T-SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) and reduced the level of malondialdehyde (MDA) in the liver. Moreover, LPT could upregulate the mRNA and protein expressions of peroxisome proliferator-activated receptor alpha (PPAR-α), lipoprotein lipase (LPL), carnitine palmitoyltransferase 1(CPT1), and cholesterol 7 alpha-hydroxylase (CYP7A1) and downregulate those of PPAR-γ and CCAAT/enhancer-binding protein alpha (C/EBP-α) in the liver. It also increased the mRNA expression of copper/zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), CAT, gamma-glutamylcysteine synthetase 1 (GSH1), and GSH-Px. The components of LPT extract include catechin, rutin, taxifolin, and astragalin, which possibly have a wide range of biological activities. In conclusion, our work verified that LPT extract possessed an anti-obesity effect and alleviated obesity-related symptoms, including lipid metabolism disorder, chronic low-grade inflammation, and liver damage, by modulating lipid metabolism and oxidative stress.

In vitro and in vivo Effects of Artesunate on Echinococcus granulosus Protoscoleces and Metacestodes.

BackgroundIn this study, we aim to investigate the efficiency of artesunate (AS) on Echinococcus granulosus protoscoleces and metacestodes.MethodsFor the in vitro assay, the eosin dye exclusion test and transmission electron microscope (TEM) were utilized to evaluate the effects of AS against protoscoleces (PSCs) from Echinococcus granulosus. In addition, mortality, ultrastructure change, reactive oxygen species (ROS) content and DNA damage were measured in order to explore the anti-echinococcosis mechanism of AS. For the in vivo assay, CE-infected mice were divided into model group, albendazole (ABZ) group (200 mg/kg), low AS (AS-L) group (50 mg/kg), moderate AS (AS-M) group (100 mg/kg), and high AS (AS-H) group (200 mg/kg). Upon 6 weeks oral administration, wet weight of cysts and the ultrastructural changes of cystic wall were utilized to evaluate the effects of AS on metacestodes. In addition, the liver biochemical parameters, tumor necrosis factor-α (TNF-α), glutathione/glutathione oxidized (GSH/GSSG) ratio in serum, and H2O2, total superoxide dismutase (T-SOD) in cyst fluid were detected.ResultsBoth in vivo and in vitro experiments showed that AS showed anti-parasitic effects on CE. The AS could elevate the ROS level in the PSCs, which then resulted in obvious DNA damages. AS could significantly improve the liver biochemical parameters in infected mice compared with the model group (P < 0.05). Compared with the model group, AS-M and AS-H decrease the TNF-α content (P < 0.05); AS-H group significantly decrease in the serum GSH/GSSG ratio (P < 0.05). The content of H2O2 in hydatid fluid treated by AS showed significant decrease compared with the model group (P < 0.01), while the T-SOD level showed significant elevation compared with model group (P < 0.01).ConclusionIn this study, we confirmed that the effects of AS on Echinococcus granulosus protoscoleces and metacestodes may be related to the DNA damages induced by oxidative stress, which provided solid information for the research and development of drugs for cystic echinococcosis.

MicroRNA-204-5p mediates sevoflurane-induced cytotoxicity in HT22 cells by targeting brain-derived neurotrophic factor.

Sevoflurane is widely used as an inhalational anesthetic in clinical practice. However, sevoflurane can cause cytotoxicity and induce learning capacity decline in patients. A previous publication indicated that miR-204-5p might have a close relationship with sevoflurane-induced neurotoxicity. When exposed to sevoflurane, the expression of miR-204-5p in neonatal hippocampus of rats was significantly increased. Hence, we aimed to investigate the role of miR-204-5p in sevoflurane-induced neurotoxicity using a mouse hippocampal neuronal cell line (HT22). The levels of miR-204-5p in HT22 cells were detected by RT-qPCR. In addition, the effects of miR-204-5p on cell viability, apoptosis and proliferation were evaluated by CCK-8, flow cytometric, and immunofluorescence assay, respectively. Western blotting was used to detect expressions of Bax, Bcl-2, active caspase 3, BDNF, TrkB, p-TrkB, Akt and p-Akt in HT22 cells. ELISA assay was used to examine the levels of total superoxide dismutase (SOD), reduced glutathione (GSH), malondialdehyde (MDA) and reactive oxygen species (ROS) in cells. Meanwhile, the dual luciferase reporter system assay was employed to explore the interaction of miR-204-5p and BDNF in cells. The level of miR-204-5p was increased in sevoflurane-treated HT22 cells. Moreover, downregulation of miR-204-5p inhibited sevoflurane-induced apoptosis and promoted cell proliferation by upregulating the proteins of Bcl-2 and downregulating the expressions of Bax and active caspase-3 in HT22 cells. In addition, inhibition of miR-204-5p alleviated sevoflurane-induced oxidative injuries in HT22 cells via decline of ROS and MDA and upregulation of SOD and GSH. Furthermore, bioinformatics and dual luciferase assay demonstrated that miR-204-5p can inhibit the TrkB/Akt pathway by targeting BDNF. Our findings indicated that downregulation of miR-204-5p can decrease oxidative status in HT22 cells and alleviate sevoflurane-induced cytotoxicity through stimulating the BDNF/TrkB/Akt pathway. Therefore, miR-204-5p might be a potential biomarker and therapeutic target for the treatment of sevoflurane-induced neurotoxicity.

Association of Cigarette Smoking With Cerebrospinal Fluid Biomarkers of Neurodegeneration, Neuroinflammation, and Oxidation

Cigarette smoking has been associated with risk of neurodegenerative disorders, such as Alzheimer disease. The association between smoking and biomarkers of changes in human cerebrospinal fluid (CSF) is not fully understood. To investigate the association of cigarette smoking with CSF biomarkers of neurodegeneration, neuroinflammation, oxidation, and neuroprotection. In this case-control study of 191 adult men in China, biomarkers in the CSF of participants with and without significant cigarette exposure were examined. Participants who did not smoke and had no history of substance use disorder or dependence were assigned to the nonsmoking group. The active smoking group included participants who consumed at least 10 cigarettes per day for 1 year. Five-milliliter samples of CSF were obtained from routine lumbar puncture conducted before anterior cruciate ligament reconstruction surgery. Data collection took place from September 2014 to January 2016, and analysis took place from January to February 2016. Cigarette smoking. CSF levels of β-amyloid 42 (Aβ42), which has diagnostic specificity for Alzheimer disease, tumor necrosis factor alpha (TNFα), brain-derived neurotrophic factor (BDNF), total superoxide dismutase (SOD), and nitric oxide synthase (NOS) were measured. Sociodemographic data and history of smoking were obtained. Of 191 participants, 87 (45.5%) were included in the active smoking group and 104 (54.4%) in the nonsmoking group. Compared with the active smoking group, the nonsmoking group was younger (mean [SD] age, 34.4 [10.5] years vs 29.6 [9.5] years; P = .01), had more education (mean [SD] duration of education, 11.9 [3.1] years vs 13.2 [2.6] years; P = .001), and had lower body mass index (mean [SD], 25.9 [3.6] vs 24.9 [4.0]; P = .005). Comparing the nonsmoking group with the smoking group, mean (SD) CSF levels of Aβ42 (38.0 [25.9] pg/mL vs 52.8 [16.5] pg/mL; P < .001) and TNFα (23.0 [2.5] pg/mL vs 28.0 [2.0] pg/mL; P < .001) were significantly lower, while BDNF (23.1 [3.9] pg/mL vs 13.8 [2.7] pg/mL; P < .001), total SOD (15.7 [2.6] U/L vs 13.9 [2.4] U/L; P < .001), total NOS (28.3 [7.2] U/L vs 14.7 [5.6] U/L; P < .001), inducible NOS (16.0 [5.4] U/L vs 10.3 [2.7] U/L; P < .001), and constitutive NOS (12.4 [6.9] U/mL vs 4.4 [3.9] U/mL) were higher. In addition, in participants in the smoking group who were aged 40 years or older, total SOD levels were negatively correlated with Aβ42 levels (r = -0.57; P = .02). In those who smoked at least 20 cigarettes per day, TNFα levels were positively correlated with Aβ42 levels (r = 0.51; P = .006). The association of TNFα with Aβ42 production was stronger than that of total SOD with Aβ42 production (z = -4.38; P < .001). This case-control study found that cigarette smoking was associated with at-risk biomarkers for Alzheimer disease, as indicated by higher Aβ42 levels, excessive oxidative stress, neuroinflammation, and impaired neuroprotection found in the CSF of participants in the active smoking group.

Structural characterization and hypoglycemic effect of green alga Ulva lactuca oligosaccharide by regulating microRNAs in Caenorhabditis elegans

The novel oligosaccharides from Ulva lactuca were obtained and characterized by nuclear magnetic resonance, Fourier-transformed infrared and liquid chromatography-quadrupole time-of-flight tandem mass spectrometry. U. lactuca oligosaccharides were composed by β-D-Glcp-(1 → 4)-α-L-Rhap (2SO3−)-(1 → 2)-β-D-GlcpA-(1 → 6)-β-D-Galp-(1 → 5)-α-L-Arap-(1→ and α-L-Rhap-(1 → 2)-α-L-Rhap(3SO3−)-(1 → 6)-β-D-Glcp-(1 → 2)-β-D-Xylp-(1→ with a branch of β-D-GlcpA that connected in C4 of β-D-Glcp, respectively. After U. lactuca oligosaccharide treatment, the mean lifespan, glucose levels, and insulin resistance were improved in Caenorhabditis elegans. It has significantly enhanced the total superoxide dismutase levels and ameliorated the intracellular reactive oxygen species accumulation. U. lactuca oligosaccharides could prevent the DNA and mitochondrial damage induced by high glucose. The gene expression levels of abnormal dauer formation 16 (DAF-16), protein kinase B (AKT-1), protein skinhead-1 (SKN-1), adenosine monophosphate-activated kinase 2 (AAK-2), DAF-15, and superoxide dismutase 3 (SOD-3) were up-regulated though inhibiting the expressions of miR-48-5p, miR-67-3p, miR-124-3p, and miR-85-3p, while the gene expression levels of DAF-2, LEThal 363 (LET-363), and signal element on X 1 (SEX-1) were also up-regulated. U. lactuca oligosaccharides might be applied in the functional foods to improve glucose metabolism disorders and antioxidant systems in vivo mediated by modulation of microRNAs.

Huoxue Huatan Decoction Ameliorates Myocardial Ischemia/Reperfusion Injury in Hyperlipidemic Rats via PGC-1α-PPARα and PGC-1α-NRF1-mtTFA Pathways.

ObjectiveThe aim of this study was to eluc\\idate the preventive and therapeutic effects and the underlying mechanisms of Huoxue Huatan Decoction (HXHT) on myocardial ischemia/reperfusion (I/R) injury in hyperlipidemic rats.MethodsAn I/R model was established in hyperlipidemic Wistar rats. After 4–8 weeks of HXHT treatment, the physical signs of rats were observed. Lipid metabolism, myocardial enzyme spectrum, cardiac function, myocardial histomorphology, and mitochondrial biosynthesis were investigated by a biochemical method, ultrasonography, electron microscopy, pathological examination, real-time PCR, and Western blot.ResultsHXHT can affect lipid metabolism at different time points and significantly reduce the levels of cholesterol (CHO), triglyceride (TG), high-density lipid-cholesterol (HDL-C), and low-density lipid-cholesterol (LDL-C) in hyperlipidemic rats (P < 0.05 or P < 0.01); it can significantly reduce the levels of creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH), reduce the myocardial infarct size and myocardial ischemic area, and improve cardiac function. The results of myocardial histomorphology showed that HXHT could protect myocardial cells, relieve swelling, reduce the number of cardiac lipid droplets, and improve myocardial mitochondrial function. HXHT could significantly increase the levels of total superoxide dismutase (T-SOD) and succinate dehydrogenase (SDH) (P < 0.05 or P < 0.01), increase CuZn-superoxide dismutase (CuZn-SOD) and glutathione-peroxidase (GSH-Px) levels, and decrease the levels of malondialdehyde (MDA) (P < 0.05); it could increase the mRNA and protein expression levels of peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (PGC-1α), peroxisome proliferator-activated receptor alpha (PPARα), nuclear respiratory factor 1 (NRF1), and mitochondrial transcription factor A (mtTFA) (P < 0.05 or P < 0.01), and increase the synthesis of mitochondrial DNA (mtDNA) (P < 0.01).ConclusionHXHT can reduce myocardial I/R injury in hyperlipidemic rats. The protective mechanisms may involve a reduction in blood lipids, enhancement of PGC-1α–PPARα pathway activity, and, subsequently, an increase in fatty acid β-oxidation, which may provide the required input for mitochondrial energy metabolism. HXHT can additionally enhance PGC-1α–NRF1–mtTFA pathway activity and, subsequently, increase the antioxidant capacity, promote mtDNA synthesis, and reduce mitochondrial damage. The two pathways use PGC-1α as the intersection point to protect mitochondrial structure and function, reduce I/R-induced injury, and improve cardiac function.

Influence of differential protein levels of feed on growth, copper‐induced immune response and oxidative stress of Rhynchocypris lagowski in a biofloc‐based system

This study compared the influences of differential protein levels of feed on growth, copper-induced digestive enzyme activity, immune response, oxidative stress and Nrf2 signalling molecules genes expression of Rhynchocypris lagowski in a biofloc-based system and traditional autotrophic system. Four hundred and fifty R. lagowski were fed four experimental dietary containing graded levels of protein from 25% to 37% (referred as biofloc technology [BFT]25, BFT29, BFT33 and BFT37, respectively) in a biofloc-based system, and 37% crude protein level (control group) were cultured in an autotrophic system in 8 weeks. At the end of the trial, there was an improvement of 50.35%–61.64% in terms of growth performance (weight gain rate); 0.25–0.53 (U/mg prot) amylase; 6.9–8.02 (U/ml) lysozyme (LZM); and 7.98–8.12 (U/ml) total superoxide dismutase (T-SOD) in R. lagowski cultured in BFT37 groups as compared to control. Obviously, the growth performance, digestive enzymes activity, immune response, antioxidant statue and antioxidant-related genes expression of R. lagowski fed with the same protein level in BFT system were significantly higher than those in the control group (p < .05). Furthermore, the level of T-SOD in liver and kidney and interferon-γ in liver of BFT33 group were also significantly higher than that of control group (p < .05). Moreover, there was no notable difference of LZM, alkaline phosphatase, complement C3, C4, heat shock proteins 70, heat shock proteins 90, insulin-like growth factor I, glutathione peroxidase, catalase, total antioxidant capacity, malondialdehyde, Ascorbic acid in gill, liver, kidney, gut and serum among the BFT29 groups and those in the control (p > .05). Besides, bioflocs assists in regulating the expression of Nrf2 signalling molecules including Nrf2, Keap1, Maf, HO-1, CAT, CuZn-SOD, GPX and GCLC. We summarized that despite the low protein content in feed, BFT system has the potential to promote growth performance, alleviate copper-induced immunosuppression and oxidative stress of juvenile R. lagowski.

Selenium Yeast Alleviates Ochratoxin A-Induced Apoptosis and Oxidative Stress via Modulation of the PI3K/AKT and Nrf2/Keap1 Signaling Pathways in the Kidneys of Chickens.

The purpose of this study was to investigate the protective effect and mechanism of yeast selenium (Se-Y) on ochratoxin- (OTA-) induced nephrotoxicity of chickens. A total of 80 one-day-old healthy chickens were randomly divided into 4 equal groups: control, OTA (50 μg/kg OTA), Se-Y (0.4 mg/kg Se-Y), and OTA+Se-Y (50 μg/kg OTA+0.4 mg/kg Se-Y). In the OTA chickens, differences in body weight, kidney coefficient, biochemical histological analysis, antioxidant capability, and the expression levels of the PI3K/AKT and Nrf2/Keap1 signaling pathway-related genes were observed. The levels of total superoxide dismutase (T-SOD), antioxidant capacity (T-AOC), catalase (CAT), and glutathione (T-GSH) significantly decreased, but the malondialdehyde (MDA) level of the kidneys significantly increased in the OTA treatment group. More importantly, treatment with Se-Y improved the antioxidant enzyme activities within the kidneys of chickens exposed to OTA. In addition, administration of OTA resulted in apoptosis and was associated with decreased expression of AKT, PI3K, and Bcl-2, which in turn enhanced expression of Caspase3, Bax, and P53. However, Se-Y improved the antioxidant defense system through activation of the Nrf2/Keap1 signaling pathway. Gene expression of Nrf2 and its target genes (HO-1, GSH-px, GLRX2, MnSOD, and CAT) was downregulated following OTA exposure. Conversely, Se-Y treatment resulted in a significant upregulation of the same genes. Besides, significant downregulations of protein expression of HO-1, CAT, MnSOD, Nrf2, and Bcl-2 and a significant upregulation of Caspase3 and Bax levels were observed after contaminated with OTA. Notably, OTA-induced apoptosis and oxidative damage in the kidney of chickens were reverted back to normal level in the OTA+Se-Y group. Taken together, the data suggest that Se-Y alleviates OTA-induced nephrotoxicity in chickens, possibly through the activation of the PI3K/AKT and Nrf2/Keap1 signaling pathways.

Bioactive peptides derived from crimson snapper and in vivo anti-aging effects on fat diet-induced high fat Drosophila melanogaster.

Crimson snapper is an important marine economy fish, and its scales are rich in collagen. Crimson snapper scale peptides (CSSPs) obtained from crimson snapper scales by enzymatic hydrolysis exhibited significantly antioxidant activities to DPPH, ABTS and hydroxyl radicals in vitro. In vivo antioxidant and anti-aging effects of CSSPs on the Drosophila melanogaster aging model constructed by lard were investigated in this study. The results showed that CSSPs could prolong the mean lifespan, 50% survival days and the maximum lifespan of Drosophila, and especially when the concentration of CSSPs was increased to 6 mg mL-1, the mean lifespan of male and female Drosophila increased by 21.2% and 26.2%, respectively, indicating the effective life extension effect of CSSPs. Meanwhile, the addition of CSSPs effectively reduced the contents of malondialdehyde (MDA) and protein carbonylation (PCO) and increased the levels of total superoxide dismutase (T-SOD) and catalase (CAT) in Drosophila, which showed a significant dose dependence. Besides, the antioxidant-related genes SOD1, SOD2 and CAT were up-regulated in Drosophila when fed with diets containing CSSPs. In conclusion, CSSPs played an antioxidant and anti-aging role by reducing the accumulation of peroxide products and improving the activity of antioxidant enzymes, as well as by up-regulating the expression of antioxidant-related genes. The results suggest that CSSPs have potential to be used in the food and healthcare industries as potential food-borne antioxidant and anti-aging agents.

Effect of Intratracheal Instillation of ZnO Nanoparticles on Acute Lung Inflammation Induced by Lipopolysaccharides in Mice.

Although studies have shown toxic effects of zinc oxide (ZnO) particles following inhalation, additional effects on injured lungs, which are characterized by dysfunction of the alveolar-capillary barriers, remain uncharacterized. To explore these additional effects, nano-sized ZnO (nZnO) and bulk-sized ZnO were applied to lipopolysaccharide (LPS)-challenged mouse lungs, which were used as a disease model of acute lung inflammation. An elevated Zn2+ concentration was detected in lung tissue after LPS plus nZnO exposure. Exposure to nZnO in LPS-challenged mice resulted in higher total cell number, proportion of neutrophils, and total protein level in bronchoalveolar lavage fluid. Intratracheal instillation of nZnO intensively aggravated LPS-induced lung inflammation that was accompanied by enhanced expression of interleukin-1β, interleukin-6, monocyte chemotactic protein-1α, and granulocyte-macrophage colony stimulating factor. Catalase, glutathione, and total superoxide dismutase levels were significantly decreased, and the malondialdehyde level was obviously increased in the LPS plus nZnO group. 8-Hydroxyguanosine, a marker for DNA damage, was highly concentrated in the lungs from the LPS plus nZnO group. Furthermore, nZnO increased lung apoptosis in an acute lung inflammation model. Taken together, this evidence indicates that nZnO aggravates lung inflammation related to LPS. This enhancement effect may be mediated via oxidative stress, which can lead to DNA damage and apoptosis. This work is important because of the ever-increasing exposure of people to ZnO nanoparticles in industry. The identification of the toxic effects of nZnO and possible mechanisms revealed in this study provide valuable information for future studies.