Expression Levels Of Superoxide Dismutase Research Articles

A study on role and mechanism of TLR4/NF-κB pathway in cognitive impairment induced by cerebral small vascular disease.

To investigate the role and potential mechanism of Toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signaling pathway in cognitive impairment induced by cerebral small vascular disease (CSVD), so as to provide a reference for the clinical treatment of CSVD-induced cognitive impairment. Mice with TLR4 gene knockout (n = 20) and those with wild-type TLR4 gene (n = 40) aged 8-10 weeks old were divided into blank control group (Control group, n = 20), wild-type + CSVD group (WT + CSVD group, n = 20) and TLR4 gene knockout + CSVD group (TLR4 KO + CSVD group, n = 20). Allogeneic thrombosis (particle diameter: 50-70 mm) was injected to the mouse's external carotid artery to create a model of learning and memory dysfunction. Step-down test and Y-type maze test were utilized to examine the learning and memory abilities of the mice. Reverse transcription-polymerase chain reaction (RT-PCR) and immunoblotting techniques were adopted to measure the levels of apoptosis-related genes [B-cell lymphoma/leukemia-2 (Bcl-2), Bcl-2-associated X protein (Bax), C-caspase-3 and T-caspase-3] in the brain tissues of mice. Terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick end labeling (TUNEL) method was applied to detect the apoptosis of neuronal cells in the brain tissues. Meanwhile, the levels of oxidative stress markers, including superoxide dismutase (SOD), gp91 and malondialdehyde (MDA), were measured. Finally, the expression level of TLR4/NF-κB pathway was detected. The latency in the step-down test in the WT + CSVD group was remarkably longer than that in the Control group, and the number of errors was evidently larger than that in the Control group (p < 0.05). At the same time, in the WT + CSVD group, the expression levels of pro-apoptotic genes Bax and C-caspase-3 were up-regulated markedly, while the expression level of anti-apoptotic gene Bcl-2 declined notably (p < 0.05). TUNEL results showed that the number of apoptotic cells in the brain tissues in the WT + CSVD group was about 12 times that in the Control group (p < 0.05). Meanwhile, the SOD expression level was lowered, and the MDA expression level was elevated in the brain tissues in the WT + CSVD group. In addition, the TLR4/NF-κB pathway was prominently activated in the mice in the WT + CSVD group (p < 0.05). After TLR4 gene knockout, the cognitive functions of the mice were improved markedly, and the apoptosis of neuronal cells and oxidative stress in the brain tissues were suppressed significantly in the meantime. Moreover, the activation of the TLR4/NF-κB signaling pathway was also inhibited. The TLR4/NF-κB pathway is involved in the occurrence and development of CSVD-induced cognitive impairment through regulating oxidative stress and cell apoptosis.

Ecotoxicological effects of transgenic mCry1Ac maize (BT799) on zebrafish

The safety of feed derived from genetically modified (GM) crops is one of the focuses of attention. To evaluate the ecotoxicological effects of transgenic mCry1Ac maize (BT799) on fish, zebrafish (Danio rerio) were fed extruded feeds containing either 20% GM maize (GMF) or its parental control maize (PF), GM maize meal (GMM) or its parental control maize meal (PMM), and a control commercial feed (CF), respectively. The growth performance, histopathology, reproduction, antioxidant enzyme activity and mRNA expression levels of sensitive protein in the liver were investigated over the course of a 98-day feeding trial. The results showed that transgenic mCry1Ac maize had no significant effect on growth, histopathology of the liver, brain and intestinal tract, fecundity, hatching rate of fertilized eggs, superoxide dismutase (SOD), catalase (CAT) activity, mRNA expression levels of SOD and CAT, or heat shock protein 70 (HSP70) and vitellogenin (VTG) in the liver. However, zebrafish fed the commercial feed exhibited significantly greater weight, longer length, and higher specific growth rate than those fed feeds (GMF and PF) and maize meals (GMM and PMM). The hatching rate of zebrafish in the feed groups was significantly lower than that of the maize meal groups and the commercial feed group. The mRNA transcriptional levels of VTG were significantly higher in the liver for the feed groups (3.85±0.76) than that for the maize meal groups (1.60±0.56). These results suggest that transgenic mCry1Ac maize has no ecotoxicological effects on zebrafish. However, the differences in nutrient composition and palatability between the extruded experimental feeds and the commercial feed would lead to significant diffe-rences in some parameters.

Effects of endurance exercise on synaptic plasticity in cerebral cortex of aged rats and related regulatory mechanism

To understand and analyze the rules of endurance exercise on the cerebral cortex adaptive mechanism in aged rats. In this study, 3-month-old (n=20), 13-month-old (n=24) and 23-month-old (n=24) specific-pathogen free (SPF) male Sprague-Dawley Rat (SD) rats were divided into young (Y-SED), middle-aged (M-SED) and old-aged (O-SED) sedentary control group, and the corresponding Y-EX, M-EX and O-EX in the endurance exercise runner group. The 10-weeks of regular moderate-intensity aerobic exercise intervention were carried out in the endurance exercise runner group. The exercise mode is treadmill exercise (slope 0), and the exercise intensity gradually increases from 60%～65% of the maximum oxygen consumption (V·O2max) to 70%～75%, and the exercise time is 10 weeks. Hematoxylin and eosin (HE) staining was used to detect age-related morphological changes. The expressions of superoxide dismutase(SOD) and brain-derived neurotrophic factor (BDNF) and the expressions of synapsin 1 (SYN1) and Ca2+/calmodulin- dependent protein kinases IIα (CaMK IIα) / AMP-activated protein kinase α1(AMPKα1) / mammalian target of rapamycin (mTOR) pathway -related genes were detected. The cerebral cortex structure of the rats in each group showed age-related aging changes, the expression of SOD in the cortex showed a gradual decline, the expression of BDNF showed an age-increasing trend, and the expression levels of SYN1 and CaMK IIα were increased with age. The changes in AMPKα1 and SirT2 and IP3R, AKT1 and mTOR mRNA levels were increased slightly in middle-aged rats and decreased in aged rats. Compared with the rats in each sedentary control group, the nucleus of the cerebral cortex was tightly arranged and the number of nuclei observed under the microscope was increased significantly in each exercise group. Exercise promoted the expressions of SOD, BDNF and synaptophysin SYN1 in the cortex of rats, and the expression levels of SOD and BDNF in aged rats were up-regulated significantly (P＜ 0.01). The expression level of SYN1 in rats was up-regulated significantly (P＜0.05) in the young and aged rats. The expression of CaMK IIα in the cortex of middle-aged and aged rats was up-regulated (P＜0.01), while the expression level of CaMK IIα in young rats was down-regulated (P＜0.01). Exercise could up-regulate the expression level of AMPKα1 in the cortex of young rats (P＜ 0.05), but not in middle-aged and old-age rats. Exercise could up-regulate the expression of SirT2 in the cortex of rats in all age groups (P＜0.05). Exercise up-regulated the expression of phosphoinositide 3-kinase (IP3R)/ protein kinase B 1(AKT1) /mTOR in the cortex of rats, among which young IP3R was significantly up-regulated (P＜0.01) in the young group, mTOR was significantly up-regulated in young and middle-aged group (P＜0.01), and mTOR was also significantly up-regulated in the aged group (P＜0.05). Endurance exercise up-regulates BDNF expression, regulates CaMKIIα signaling, activates AMPK signaling pathway and IP3R / AKT1 / mTOR signaling pathway, and improves synaptic plasticity in the cortex.

Bioaccumulation and physiological responses in juvenile Marsupenaeus japonicus exposed to cadmium

The heavy metal cadmium readily accumulates in organisms, causing damage. In this study, juvenile marine shrimp Marsupenaeus japonicus were exposed to cadmium (Cd2+; 5, 50 and 500 μg L–1). Cd accumulation and antioxidant-related indices were determined, and damage to biomolecules was assessed, after 24, 48 and 96 h. Cd bioaccumulation in M. japonicus increased with exposure time and concentration, which reached the highest value at 96 h. The data showed that 5, 50 and 500 μg L–1 Cd increased glutathione (GSH) content and the activities of superoxide dismutase (SOD) and glutathione S-transferase (GST) in a Cd-dose-dependent manner, but 5 and 50 μg L–1 Cd had no effect on caspase-3 activity. The expression levels of SOD, GST, heat shock protein 70 (HSP70), metallothionein (MT), p53 and caspase-3 genes were rapidly increased after 50 and 500 μg L–1 Cd exposure, and remained at a significantly higher level than in the control after 96 h of exposure. After exposure to 5, 50 and 500 μg L–1 Cd, F-value (the ratio between double-stranded DNA and total DNA) remained high at 24 h, however, as the exposure time increased, the F-value decreased in a dose-dependent manner. An increase in malondialdehyde content was also observed following exposure to 50 and 500 μg L–1 Cd. Our data suggest that Cd induces oxidative stress, molecular damage and apoptosis in juvenile M. japonicus in a concentration- and time-dependent manner.

Effect of Telmisartan in the Oxidative Stress Components Induced by Ischemia Reperfusion in Rats.

The therapeutic effects of telmisartan, an angiotensin II receptor antagonist and a peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist, have been demonstrated in several disorders. It has antioxidant and immune response modulator properties and has shown promising results in the treatment of an ischemia/reperfusion (I/R) lesion. In this study, a skeletal muscle (right gastrocnemius muscle) I/R lesion was induced in rats and different reperfusion times (1 h, 24 h, 72 h, 7-day, and 14-day subgroups) were assessed. Furthermore, levels of oxidative markers such as enzymatic scavengers (catalase (CAT) and superoxide dismutase (SOD)) and metabolites (nitrates and 8-oxo-deoxyguanosine) were determined. The degree of tissue injury (total lesioned fibers and inflammatory cell count) was also evaluated. We observed an increase in CAT and SOD expression levels under telmisartan treatment, with a decrease in injury and oxidative biomarker levels in the 72 h, 7-day, and 14-day subgroups. Telmisartan reduced oxidative stress and decreased the damage of the I/R lesion.

Protective effect of folic acid on vulnerability to oxidative stress in dental pulp stem cells of deciduous teeth from children with orofacial clefts

Orofacial clefts (OFCs) are among the most common congenital craniofacial malformations, including cleft lip with or without cleft palate as the core symptoms. Developmental or functional defects in neural crest cells (NCCs) that contribute to craniofacial morphogenesis are involved in OFC development. Previous studies have suggested that oxidative stress in NCCs is involved in the development of OFCs, suggesting that the anti-oxidative activity of folic acid (FA) could have protective effects. However, studies of human-derived NCCs are limited, as these cells are predominantly active during the embryonic stage. In this study, the effects of oxidative stress and FA were evaluated in human OFCs. In particular, NCC-derived stem cells from human exfoliated deciduous teeth (SHEDs) were obtained from 3 children with non-syndromic cleft lip with cleft palate (CLPs) and from 3 healthy children (CTRLs). Mitochondrial reactive oxygen species (ROS) levels were significantly higher in CLPs than in CTRLs and were associated with lower mRNA expression levels of superoxide dismutase 1 (SOD1) and decreased cell mobility. In addition, significantly greater vulnerability to pyocyanin-induced ROS, mimicking exogenous ROS, was observed in CLPs than in CTRLs. These vulnerabilities to endogenous and exogenous ROS in CLPs were significantly improved by FA. These results indicated that the transcriptional dysregulation of SOD1 in NCCs is an oxidative stress-related pathological factor in OFCs, providing novel evidence for the benefits of perinatal anti-oxidant supplementation, including FA, for the management of these common deformities.

Effects of Sevoflurane Pretreatment on Myocardial Ischemia-Reperfusion Injury Through the Akt/Hypoxia-Inducible Factor 1-alpha (HIF-1α)/Vascular Endothelial Growth Factor (VEGF) Signaling Pathway.

BackgroundThe aim of this study was to investigate the effects of sevoflurane (SEV) on myocardial ischemia/reperfusion (I/R) injury in rats and its mechanism.Material/MethodsSixty male Sprague-Dawley rats were randomly divided into 3 groups: Sham group (n=20), I/R group (n=20) and I/R+SEV group (n=20). The I/R model was established by ligating and recanalizing the left anterior descending coronary artery (LAD). Triphenyl tetrazolium chloride (TTC) test and echocardiography (ECG) were used for analysis. Hematoxylin and eosin (H&E) staining was applied to detect the morphological changes. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining was conducted to detect the apoptosis levels. The expression level of superoxide dismutase 2 (SOD2) was measured. Finally, the effect of SEV on the protein kinase B (Akt)/hypoxia-inducible factor 1-alpha (HIF-1α)/vascular endothelial growth factor (VEGF) signaling pathway was detected via western blotting.ResultsSEV could significantly improve I/R-induced cardiac insufficiency, inhibit cardiac infarction, and as well as reduce the infarction area from 53.21±2.11% to 32.33±3.49% (P<0.05). Compared with rats in I/R group, the cardiac myofilament was better in alignment, degradation and necrosis were milder, and cell edema was notably reduced in the I/R+SEV group. Thus, SEV could significantly reverse the decreased expression of SOD2 caused by I/R and reduce oxidative stress in the heart (P<0.05). According to the western blotting results, SEV was capable of obviously activating the expressions of phosphorylated-Akt (p-Akt), HIF-1α, and VEGF.ConclusionsSEV can significantly improve myocardial injury caused by I/R in rats, and its mechanism might be related to the activation of the Akt/HIF-1α/VEGF signaling pathway.

Effects of silymarin on growth performance, antioxidant capacity and immune response in turbot (Scophthalmus maximus L.)

AbstractA 9‐week feeding trial was conducted using triplicate groups of turbot (6.50 ± 0.01 g) to explore the potential effects of silymarin. Three concentrations of silymarin (100, 200, and 400 mg/kg) were added to the plant protein‐based diet. Fish were randomly distributed into fiberglass tanks (30 fish per tank). The results showed that adding 100 mg/kg silymarin significantly improved the growth performance, with no effects on feed utilization. The antioxidant capacity in the liver was significantly improved in the 100 mg/kg and 200 mg/kg silymarin groups by not only inducing the activities of superoxide dismutase (SOD) and catalase but also increasing the messager RNA (mRNA) expression levels of SOD, glutathione peroxidase, and peroxiredoxin 6. Meanwhile, supplying 100 and 200 mg/kg of silymarin enhanced the heights of villi and enterocytes. Silymarin supplementation reduced the mRNA expression of interleukin‐8 and tumor necrosis factor‐α but induced the expression of transforming growth factor‐β (TGF‐β) in the intestine. These results indicated that silymarin was a potential nutraceutical that could enhance the growth performance and health status of turbot fed in a high plant protein diet. Adding 100 mg/kg silymarin to the plant protein diet achieved optimal performance in turbot.

Effects of Asiaticoside Treatment on the Survival of Random Skin Flaps in Rats

Background: Asiaticoside (AS) is extracted from the traditional herbal medicine Centella asiatica, and has angiogenic, antioxidant, anti-inflammatory, and wound-healing effects. We investigated the effects of AS on skin flap survival. Methods: Dorsal McFarlane flaps were harvested from 36 rats and divided into two groups: an experimental group treated with 40 mg/kg AS administered orally once daily, and a control group administered normal saline in an identical manner. On day 2, superoxide dismutase (SOD) and malondialdehyde (MDA) levels, and production of the cytokines tumor necrosis factor-α and interleukin (IL)-6 were evaluated. On day 7, tissue slices were stained with hematoxylin and eosin. The expression of vascular endothelial growth factor (VEGF), IL-6, and IL-1β were immunohistochemically evaluated. Microcirculatory flow was measured using laser Doppler flowmetry. Flap angiography, using the lead oxide-gelatin injection technique, was performed with the aid of a soft X-ray machine. Results: The AS group exhibited greater mean flap survival area, improved microcirculatory flow, and higher expression levels of SOD and VEGF compared with the control group. However, MDA levels and the inflammatory response were significantly reduced. Conclusions: AS exhibits promise as a therapeutic option due to its effects on the viability and function of random skin flaps in rats.

Effect of Sheng-jiang powder on multiple-organ inflammatory injury in acute pancreatitis in rats fed a high-fat diet.

BACKGROUNDObesity worsens inflammatory organ injury in acute pancreatitis (AP), but there is no effective preventive strategy. Sheng-jiang powder (SJP) has been shown to alleviate multiple-organ inflammatory injury in rats with high-fat diet-induced obesity. Hence, SJP is supposed to have an effect on multiple-organ inflammatory injury in AP in rats fed a high-fat diet.AIMTo explore how obesity may contribute to aggravating inflammatory organ injury in AP in rats and observe the effect of SJP on multiple-organ inflammatory injury in AP in rats fed a high-fat diet.METHODSRats were randomly assigned to a control group (CG), an obese group (OG), and an SJP treatment group (SG), with eight rats per group. The rats in the OG and SG were fed a high-fat diet. From the third week, the rats in the SG were given oral doses of SJP (5 g/kg of body weight). After 12 wk, AP was induced in the three groups. Serum amylase level, body weight, Lee’s index, serum biochemistry parameters, and serum inflammatory cytokine and tissue cytokine levels were assessed, and the tissue histopathological scores were evaluated and compared.RESULTSCompared with the CG, serum triglyceride, total cholesterol, interleukin-6, and interleukin-10 levels were significantly higher in the OG, and serum high-density lipoprotein cholesterol level was significantly lower in the OG. Moreover, enhanced oxidative damage was observed in the pancreas, heart, spleen, lung, intestine, liver, and kidney. Evidence of an imbalanced antioxidant defense system, especially in the pancreas, spleen, and intestine, was observed in the obese AP rats. Compared with the OG, serum high-density lipoprotein cholesterol, interleukin-10, and superoxide dismutase expression levels in the pancreas, spleen, and intestine were increased in the SG. Additionally, SJP intervention led to a decrease in the following parameters: body weight; Lee’s index; serum triglyceride levels; serum total cholesterol levels; malondialdehyde expression levels in the pancreas, heart, spleen, lung, and liver; myeloperoxidase expression levels in the lung; and pathological scores in the liver.CONCLUSIONObesity may aggravate the inflammatory reaction and pathological multiple-organ injury in AP rats, and SJP may alleviate multiple-organ inflammatory injury in AP in rats fed a high-fat diet.

Antioxidant responses to salinity stress in an invasive species, the red-eared slider (Trachemys scripta elegans) and involvement of a TOR-Nrf2 signaling pathway

The red-eared slider (Trachemys scripta elegans), a freshwater turtle, is an invasive species in many parts of the world where it survives in both freshwater and coastal saline habitats. High salinity can induce reactive oxygen species (ROS) production and lead to oxidative damage. In this study, we investigate the antioxidant defense mechanisms of T. s. elegans in response to salinity stress. The results showed that the mRNA expression levels of superoxide dismutase (SODs), catalase (CAT) and glutathione peroxidase (GSH-PXs) were significantly increased in both 5 psu and 15 psu groups at the early stages of salinity exposure (generally 6–48 h), but typically returned to control levels after the longest 30 d exposure. In addition, hepatic and cardiac mRNA levels of the NF-E2-related factor 2 (Nrf2), showed a similar upregulation as an early response to stress, but decreased at 30 d in the 5 psu and 15 psu groups. The mRNA levels of the negative regulator of Nrf2, kelch-like ECH associating protein 1 (Keap1), exhibited the opposite pattern. Moreover, mRNA expression levels of target of rapamycin (TOR) and ribosomal protein S6 kinase 1 (S6K1) in liver and heart showed roughly similar patterns to those for Nrf2. Furthermore, the content of malondialdehyde (MDA) was significantly increased in liver, especially in the 15 psu group by ~2.5-fold. Taken together, these results indicate that T. s. elegans may activate the TOR-Nrf2 pathway to modulate antioxidant genes transcription in order to promote enhanced antioxidant defense in response to salinity stress.

Effects of Pistacia atlantica on Oxidative Stress Markers and Antioxidant Enzymes Expression in Diabetic Rats

Introduction: Diabetes mellitus (DM) affects many patients all over the world. It involves different parts of the body, such as brain, eyes, kidneys, vessels, and so on. The lack of balance between free radicals and antioxidants is a possible mechanism involved in the pathogenesis of diabetes. Antioxidant treatment, especially natural forms, can be a beneficial solution. Therefore, we evaluated the effects of Pistacia atlantica oleoresin (PAO) on oxidative stress markers and antioxidant enzymes expression in diabetic rats.Method: Fifty adult male Wistar rats were allotted randomly into five groups as follow: control group, diabetic control group, glibenclamide control group, diabetic glibenclamide group, diabetic treated group with 200 mg/kg PAO. Then PAO was prepared and analyzed by gas chromatography/mass spectroscopy (GC/MS). LD50 was also estimated for essential oil. Oxidative stress markers and antioxidant enzyme including malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD) were also measured. The expression of GPx, CAT, and SOD genes was investigated using real-time polymerase chain reaction (PCR).Results: The main constituents of essential oil gum were beta-pinene (29.38%), followed by alpha-pinene (18.15%), myrcene (7.36%), trans-pinocarveol (7.15%), and camphene (4.12%). Diabetes induced an increased level of MDA (69.92 ± 3.92 vs. 43.76 ± 3.73) and decreased levels of GSH (2.57 ± 0.40 vs. 7.05 ± 1.59), GPx (11.66 ± 2.2 vs. 16.38 ± 2.1), CAT (12.17 ± 3.38 vs. 18.7 ± 2.66), and SOD (0.78 ± 0.67 vs. 2.41 ± 0.46). In contrast, PAO treatment significantly decreased MDA (54.59 ± 12.54 vs. 69.92 ± 3.92) and increased GSH (4.5 ± 0.89 vs. 2.57 ± 0.40), GPx (25.86 ± 5.37 vs. 11.66 ± 2.2), CAT (22.69 ± 0.36 vs. 12.17 ± 3.38), and SOD (3.65 ± 1.08 vs. 0.78 ± 0.67) (p < 0.05). Moreover, our results indicated that both GPx and CAT mRNA levels significantly increased approximately 4.46 and 6.23 times in rats fed with 200 mg/kg of PAO, more than that of the healthy control group, respectively (p < 0.01 and p < 0.001, respectively). Also, the average expression level of SOD was also significantly 1.57 higher in rats fed with 200 mg/kg of PAO in comparison to the diabetic control group (p < 0.05).Conclusion: The results indicated that PAO could be propose as an agent that protects the body against diseases that are associated with oxidative stress.

Icariin protects vascular endothelial cells from oxidative stress through inhibiting endoplasmic reticulum stress

ObjectiveTo investigate the protective effect and underlying mechanism(s) of icariin (ICA) in preventing hydrogen peroxide (H2O2)-induced vascular endothelial cell injury via endoplasmic reticulum stress (ERS). MethodsTo study the effects of ICA on H2O2-induced damage, we used the cell counting kit-8 assay to detect cell viability and the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay to determine cell adhesion and apoptosis, respectively. Spectrophotometry and enzyme-linked immunosorbent assay were used to measure the expression levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Subsequently, glucose-regulated protein 78 (GRP78), activating transcription factor-4 (ATF4) and eukaryotic initiation factor-2α (eIF2α) were detected using Western blotting. ResultsIn human umbilical vein endothelial cells, different concentrations of ICA exhibited multiple effects, including reduced H2O2 damage, improved cell viability and adhesion, reduced cell apoptosis and increased SOD and GSH-Px activity. Among the ICA concentrations used, only the H2O2 + 100 μmol/L ICA group had significant differences compared to the H2O2 group. ERS activators H2O2 and dl-dithiothreitol (DTT) significantly increased GRP78, ATF4 and eIF2α expressions, decreased cell activity and reduced SOD and GSH-Px activity. In contrast, the H2O2 + 100 μmol/L ICA and H2O2 + 100 μmol/L ICA + DTT groups had significant inhibitory effects on the expressions of GRP78, ATF4 and eIF2α proteins, showing enhanced cell viability and SOD and GSH-Px activity. ConclusionThe results showed the dose-dependent effects of ICA against H2O2-induced injury in vascular endothelial cells. The inhibition of GRP78, ATF4 and eIF2α protein expressions in the ERS, and the subsequent alleviation of oxidative stress damage, might be the molecular mechanism.

The effect of Spirulina platensis meal on antioxidant gene expression, total antioxidant capacity, and lipid peroxidation of rainbow trout (Oncorhynchus mykiss).

The study was conducted to investigate the effect of diets containing 0, 2.5, 5, 7.5, and 10% S. platensis meal on total antioxidant capacity (TAC) and lipid peroxidation, as well as the expression of two antioxidant enzyme genes (SOD and CAT) in rainbow trout (Oncorhynchus mykiss). One hundred and eighty fish, with an average initial weight of 101 ± 8g, were cultured for 10weeks. At the end of experiment, lipid peroxidation significantly decreased in serum of fish fed with S. platensis and fish fed with 5, 7.5, and 10% microalgae showed a significantly lower value compared to control and 2.5%. Inclusion of 7.5 and 10% S. platensis in diet also decreased lipid peroxidation in liver. TAC significantly increased with increasing level of S. platensis. Expression level of superoxide dismutase (SOD) and catalase (CAT) genes significantly increased in the fish liver after administration of microalgae and fish fed with 10% S. platensis in diet showed the highest level compared to the other treatments. The present study reveals that inclusion of 10% S. platensis in diet can decrease oxidative stress in rainbow trout. Therefore, S. platensis can be used as potential antioxidant for fish farming.

The involvement of the mGluR5-mediated JNK signaling pathway in rats with diabetic retinopathy.

To understand the involvement of the mGluR5-mediated JNK signaling pathway in rats with diabetic retinopathy (DR). This study established rat models of diabetes mellitus (DM), which were divided into Normal, DM, DM + CHPG (mGluR5 agonist CHPG), and DM + MTEP (mGluR5 antagonist MTEP) groups. The blood glucose and weight of rats were recorded. EB staining was used for observation of blood-retinal barrier (BRB) damage. Neural retina function was measured by pattern electroretinogram (ERG). PAS and NG2 immunohistochemistry were conducted to evaluate the retinal vascular morphology. The TUNEL assay and active caspase-3 immunohistochemistry were performed to detect retinal cell apoptosis. Additionally, the expression levels of superoxide dismutase (SOD) and methylenedioxyamphetamine (MDA) were measured. Moreover, expression levels of mGluR5 and JNK pathway-related proteins were detected by western blot. When compared with control rats, rats in the DM group showed decreased amplitude and latency of the peak times in the ERG test; further, DM group rats presented increases in blood glucose, BRB permeability, a retinal capillary area density, retinal cell apoptosis with an increased number of active caspase-3-positive cells, MDA level, mGluR5 levels, and the ratio of p-JNK/JNK, and they showed reductions in body weight and SOD activity, as well as in the number of pericytes and in the pericyte coverage (all P < 0.05). However, rats in DM + CHPG group had stronger negative effects than those in DM group (all P < 0.05). Rats from DM + MTEP group showed an opposite trend compared with the DM rats (all P < 0.05). The level of mGluR5 in DR rats was upregulated, whereas inhibition of mGluR5 alleviated retinal pathological damage and decreased cell apoptosis to improve DR via suppression of the JNK signaling pathway, which provided a scientific theoretical basis for the clinical treatment of DR.

Inhibition of histone deacetylase protects the damaged cataract via regulating the NF-κB pathway in cultured lens epithelial cells

Induction of oxidative damage by the activation of histone deacetylase (HDAC) is an integral event that causes major membrane damage of ocular tissues and leads to the pathogenesis of cataract. It is elucidated that nuclear factor-κB is a mediator in the process of cataract development. However, studies on the role played by epigenetic proteins in regulating cataract pathogenesis are limited. Hence, in the current investigation, ARPE-19 human retinal epithelial cells were used as an experimental model to elucidate the role of HDAC inhibition and its mechanism behind the cataract pathogenesis. ARPE-19 cells were exposed to H2O2, with and without Trichostatin A (TSA), a pan-HDAC inhibitor, and maintained along with control cells without any treatment. On exposure to H2O2, cells were susceptible to oxidative stress as it is evident from the reduced expression levels of superoxide dismutase (SOD), catalase, and GSH levels. Simultaneously, H2O2-exposed cells showed the nuclear translocation of NF-κB with the activation of inflammatory cytokines such as CXCL1 and IL-6. In addition, the mRNA expression analysis revealed that the GADD45α, COX-2, MCP-1, and ICAM-1 expressions were increased in H2O2 group. Moreover, the activity of HDAC was increased to 2-fold with a significant reduction in the histone acetyltransferase (HAT) activity in cells that were maintained under oxidative conditions. However, TSA was able to inhibit the critical cytokines’ expression with attenuated HDAC activity and limited NF-κB translocation. Furthermore, pre-treatment of TSA significantly suppressed the transcript levels of up-regulated inflammatory markers in cells. Together, these findings offer new insight into the role of HDACs in regulating cellular processes involved in the pathogenesis of cataract as well as the potential use of HDAC inhibitors as therapeutics for controlling the disease progression.

Modulatory effect of baicalein on gene expression and activity of antioxidant enzymes in streptozotocin-nicotinamide induced diabetic rats

Oxidative stress plays the central role in the pathogenesis and progression of diabetic complications. The present study aims to investigate the beneficial effect of oral administration of flavone baicalein in streptozotocin-nicotinamide (STZ-NA) induced diabetic rats by measuring oxidative stress markers, antioxidant enzyme activities and expression analysis of antioxidant genes. Experimental diabetes was induced by a single intraperitoneal (i.p.) injection of STZ (55 mg /kg b.wt), 15 min after the i.p. administration of NA. At the end of the experimental period, thiobarbituric acid reactive substances (TBARS), activities of antioxidant enzymes and expression levels of superoxide dismutase (SOD), catalase (CAT), glutathione (GSH) and glutathione peroxidase (GPx) were measured in diabetic rats along with serum biochemical parameters namely total cholesterol (TC), total triglyceride (TG), aspartate transaminase (AST) alanine transaminase (ALT) and glycosylated hemoglobin (HbA1c). Oral administration of baicalein (40 mg/kg b.wt/day) demonstrated a significant ameliorative effect on all studied biochemical and oxidative stress parameters. Biochemical findings were corroborated by qPCR expression analysis which showed significant upregulation of antioxidant genes in diabetic rats. These results suggest that baicalein supplementation may reduce diabetes and its complications by suppressing oxidative stress and enhancing gene expression and antioxidant enzyme activities in diabetic rats.

Effect of Clostridium butyricum in different forms on growth performance, disease resistance, expression of genes involved in immune responses and mTOR signaling pathway of Litopenaeus vannamai

A 42-day feeding trial was conducted to evaluate the effects of diet supplemented with various additives from Clostridium butyricum (fermentation supernatant, FS; live cells, LC; cell-free extract, CE; spray-dried spores, DS; mixture of live cells and supernatant, LCS) on the growth, intestinal morphology, disease resistance, immune gene expression and mTOR signaling-related gene expression in Litopenaeus vannamai. The feeding trial showed that the final weight and specific growth rate of the shrimp were improved significantly while the feed conversion ratio were reduced significantly in LC, CE, DS and LCS groups compared to the control. The villus height and intestinal wall thickness of shrimp's mid-intestine in LC, DS and LCS group increased significantly. After challenge test to Vibrio parahaemolyticus, the cumulative mortalities of the shrimp in LC, CE, DS and LCS groups were significantly lower than that of the control. As compared to the control, the relative expression levels of superoxide dismutase, lysozyme, prophenoloxidase (proPO), Toll, Immune deficiency (Imd), Relish, TOR, 4E-BP, eIF4E1α and eIF4E2 genes in the shrimp of DS and LCS groups enhanced significantly, whereas the relative expression levels of proPO, SOD, Toll, Imd, Relish, elF4E1α and elF4E2 genes were statistically the same between FS group and the control. These results suggested that the spray-dried spores and mixture of live cells and supernatant of C. butyricum exerted better probiotic benefits in modulating immune responses of shrimp. In addition, single supernatant could not be helpful to shrimp while mixture of live cells and supernatant could better improve the immune responses of shrimp in comparison to single live cells. The integration of C. butyricum and their metabolites supplemented into feed could significantly improve growth performance, intestinal morphology, immunity capacity and resistance against V. parahaemolyticus of L. vannamei.

IL-9 exacerbates the development of chronic obstructive pulmonary disease through oxidative stress.

To investigate the role of IL-9 in chronic obstructive pulmonary disease (COPD), and to explore its potential mechanism. A mouse COPD model was established by exposure to cigarette smoke. COPD mice were then randomly assigned into two groups, including: the PBS group and the IL-9 antibody group. The above two groups were treated with phosphate-buffered saline (PBS) or IL-9 injection, respectively. The histopathological changes in lung tissues of mice were observed by hematoxylin-eosin (H&E) staining. Immunohistochemistry was performed to detect IL-9-positive (IL-9+) cells in lung tissues. Expression levels of IL-9, sIL-9R, STAT3, and p-STAT3 in peripheral blood of mice were determined by quantitative Real time-polymerase chain reaction (qRT-PCR), enzyme-linked immunosorbent assay (ELISA), and Western blot, respectively. In addition, the expression levels of superoxide dismutase (SOD), malondialdehyde (MDA), and reactive oxygen species (ROS) were detected. H&E staining results showed that the airway wall structure of COPD mice in the PBS group was irregular. Ciliated columnar epithelium exhibited marked degeneration, necrosis and shedding. Besides, numerous inflammatory cell infiltration, narrowing and rupture of the alveolar septa, and larger cysts fused by adjacent alveoli were observed. H&E staining also indicated that the structure of alveolar epithelium was severely impaired in COPD mice. However, the pathological changes in lung tissues of mice in the IL-9 antibody group were much milder than those of the PBS group. Immunohistochemistry results showed a significant deposition of IL-9+ cells in the lung tissues of the PBS group. Meanwhile, the mRNA and protein levels of IL-9, sIL-9R, and p-STAT3 in the PBS group were also remarkably higher than those of the IL-9 antibody group. In addition, SOD content in the PBS group was significantly decreased, whereas the levels of MDA and ROS were significantly increased than those of the IL-9 antibody group. IL-9 activated STAT3 and aggravated lung injury in COPD mice by increasing inflammatory and oxidative stress.

Spermidine application alleviates salinity damage to antioxidant enzyme activity and gene expression in alfalfa.

We investigated whether spermidine (Spd) application alleviates salinity-induced damage in alfalfa (Medicago sativa L), and explored defence mechanisms associated with stress-related ion balance, antioxidant metabolism, and gene expression. We examined the response of 30-day-old alfalfa maintained in hydroponic culture tests for 7 days and subjected to one of six treatments: half-strength Hoagland solution (control); 1% NaCl; 10 μM Spd + 1% NaCl; 20 μM Spd + 1% NaCl; 40 μM Spd + 1% NaCl; and 60 μM Spd + 1% NaCl. In salinity-stressed plants, chlorophyll b, chlorophyll a + b, and total protein showed significant decreases, while marked increases were detected in relative electrolyte leakage, H2O2 content, glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), peroxidase (POD), glutathione reductase (GR) activity, the Na+/K+ ratio, and APX1, APX2, GR, and SOD gene expression levels. Chlorophyll a and total protein content markedly increased under exogenous application of 20 μM Spd, while H2O2 content, GSH, SOD, CAT, POD, GR activity, the Na+/K+ ratio, and APX2, GR, and SOD expression levels all decreased. These results indicated that exogenous application of 20 μM spermidine effectively alleviates salinity-induced damage in alfalfa. These findings could benefit alfalfa cultivation and promote the development and utilization of saline-alkali soil.