Decreased Superoxide Dismutase Activity Research Articles

The effect of subchronic cigarette smoke exposure on oxidative stress parameters and endothelial nitric oxide synthase in a rat aorta.

BACKGROUNDThe compounds in cigarette smoke are believed to cause oxidative stress, leading to endothelial dysfunction. Understanding the mechanism of endothelial dysfunction due to cigarette smoke is useful for the development of early and preventive therapy for cardiovascular diseases (CVDs) with smoking risk factors.METHODSIn this experimental study, a posttest-only control group design was used. 20 Wistar rats were divided into two groups: a smoking group (exposed to 40 cigarettes per day for 4 weeks) and a control group. After the exposure, the animals were sacrificed and aortas were removed for measurement of malondialdehyde (MDA), superoxide dismutase (SOD), endothelial nitric oxide synthase (eNOS), intima-media thickness (IMT), and for histological analysis.RESULTSExposure to cigarette smoke caused a significant decrease in SOD activity (24.28 ± 4.90; P = 0.027) and eNOS levels (50.81 ± 4.18; P = 0.014), but no significant effect on the level of MDA (17.08 ± 5.78; P = 0.551). Histological analysis showed an increase in IMT (13.27 ± 2.40; P = 0.000) and disorganization and vacuolation of smooth muscle cells in tunica media after exposure to cigarette smoke. The regression analysis showed a significant negative relationship between the eNOS level and IMT (β = -1.012, P = 0.009).CONCLUSIONSubchronic exposure to cigarette smoke caused a decrease in SOD activity and eNOS levels, but no significant change in MDA levels. This study also indicated that smoking causes IMT thickening and pathological structural changes in the aorta. Another finding indicated that a decrease in eNOS levels could cause an increase in the IMT of the aorta.

Shenlian extract attenuates TNF-α-induced ECV304 injury by regulating Nrf2/Keap1 signaling pathway

This study aimed to investigate the effect and the possible mechanism of Shenlian( SL) extract on tumor necrosis factor-α( TNF-α)-induced ECV304 injury. After the establishment of TNF-α-induced ECV304 cells injure model,MTT assay was used to detect cell viability and the level of reactive oxygen species( ROS) was measured by flow cytometry. The contents of superoxide dismutase( SOD),malondialdehyde( MDA),nitric oxide( NO),endothelin-1( ET-1) and interleukin-1β( IL-1β) in the supernatant were detected by biochemical method and enzyme linked immunosorbent assay( ELISA). The expression levels of apoptosis-related proteins B-lymphoma-2 gene( Bcl-2),Bcl-2 associated X protein( Bax),caspase-3,caspase-9 and nuclear factor E2 associated factor2( Nrf2)/Kelch like epichlorohydrin associated protein-1( Keap1) signaling pathway related proteins Nrf2,Keap1,quinone oxidoreductase( NQO1) and heme oxygenase 1( HO-1) were detected by Western blot. The results showed that 50 μg·L-1 TNF-α significantly damaged ECV304 cells,induced the impairment of cell viability( P<0. 01),the increase of ROS production,the decrease of SOD activity,and the increase of MDA,NO,ET-1 and IL-1β( P<0. 01),meanwhile,it caused the up-regulation of Keap1,caspase-9 and Bax protein expression,and down-regulation of NQO1 and Bcl-2 protein expression( P<0. 05) compared with the control group.Compared with the model group,SL extract reduced the damage of ECV304 cells induced by TNF-α,improved cell viability,reduced ROS production,increased SOD activity and decreased MDA,NO,ET-1,IL-1β content( P<0. 01 or P<0. 05). In addition,SL extract also down-regulated the protein expression levels of Keap1,caspase-3,caspase-9 and Bax,and increased the protein expressions of Nrf2,NQO1,HO-1 and Bcl-2( P<0. 01 or P<0. 05). The above results indicate that SL extract can provide protective effect on ECV304 cells injury induced by TNF-α,alleviate oxidative stress injury,inflammation and apoptosis,and its mechanism may be related to regulating Nrf2/Keap1 signaling pathway.

Effects of Metformin on Experimental Varicocele in Rats.

The current study aimed to determine the effect of metformin (MET) on histopathologic evaluation and antioxidant enzyme activity in experimental varicocele-induced rats. A total of 60 rats were randomly divided into six experimental groups. Group 1 (control) received no medication and underwent no surgery. In group 2 (sham), the rats received no medication and the abdominal cavity was opened; however, there was no varicocele induction. In group 3 (varicocele), the abdominal cavity was opened and the rats underwent varicocele induction and received no medication. In group 4, the abdominal cavity was opened and the animals received 25 mg/kg of MET for 42 days and were varicocele-induced. Groups 5 and 6 were similar to group 4 except that the animals received 50 and 100 mg/kg of MET, respectively. At the end of the 21st and 42nd days, the rats were euthanized and the left testis was removed for histological analysis and measurement of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GPx), and total antioxidant status levels. According to the results, a dose-dependent difference was observed in testis damage grade in the MET treated groups, compared to that reported for the varicocele group (p <0.05). No difference was observed between 25 and 50 mg/kg of MET (P>0.05). Tissue MDA levels significantly increased in varicocele rats (p <0.05); however, MET (25, 50, and 100 mg/kg) in a dose-dependent manner decreased varicocele-induced MDA (p <0.05). Experimental varicocele significantly decreased SOD activity, compared to that reported for the control group (p <0.05). The administration of MET (25, 50, and 100 mg/kg) significantly increased tissue SOD activity in varicocele rats (p <0.05). The MET (25, 50, and 100 mg/kg) in a dose-dependent manner increased GPx activity in varicocele rats (p <0.05). There was no difference in MDA, SOD, and GPx levels between 25 and 50 mg/kg MET groups (P>0.05). The aforementioned findings suggested that MET treatment had beneficial effects on varicocele.

Biochemical composition changes of gram-negative microorganisms under the action of new chemical compounds

Introduction. It is known that the enzymes catalase (CT) and superoxide dismutase (SOD) are actively involved in protecting cells of microbial pathogens against the biochemical factors produced by macrophages in vivo, in order to stop infection. Therefore, this study was aimed to quantify the parameters of the antioxidant-enzyme activities within the reference cultures under the action of selected new chemical compounds.Material and methods. Cu (II) coordination compounds, Co (II) and Zn (II) were included as “in vitro” study material, as well as aromatic propenones synthesized at the Department of Inorganic Chemistry, at State University of Moldova. The antimicrobial effects were tested on three gram-negative reference strains. The enzymatic activity of SOD and the CT activity was determined to assess the pathogen-induced changes in the antioxidant status under the action of newly tested compounds.Results. The new chemical compounds showed a significant decrease in the antioxidant enzymatic activities of SOD and CT, induced in all reference strains used, which indicates an intense oxidative stress generated by the tested compounds.Conclusions. The specific activity of new chemical compounds on primary antioxidant enzymes, which represent pathogenicity factors of infectious agents, allows us to assume the benefits of in vivo effect of new native substances, as well as to recommend the selected compounds for further biomedical tests.

Effect of subacute oral exposure to calcium carbide (CaC2) on some haematobiochemical parameters in male Wistar rats

Introduction: One of the most common methods of forced ripening of fruits involves the use of calcium carbide (CaC2). Commercial grade CaC2 contains impurities with the potential to cause harmful effects to exposed individuals. This study was conducted to determine the effect of exposure to CaC2 on some haematological and biochemical parameters in rats. Methods: Adult male Wistar rats (n=20) were divided into four equal groups. Animals in Groups I (control), II, III and IV were respectively administered distilled water (2 mL/kg), 125, 250 and 500 mg/kg calcium carbide, orally, by gavage, before feeding, daily for 28 days. The erythrogram, leucogram and plasma total protein were determined, while changes in serum and brain biomarkers of oxidative stress (superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration) were assessed. Weight changes at the beginning and at the end of the exposure period (28 days) and signs of toxicity daily, were recorded. Results: The findings revealed significantly (p<0.05) lowered levels of red blood cells count (RBC count), haemoglobin and total white blood cells count (TWBC) in the rats exposed to CaC2. How-ever, the packed cell volume (PCV) was not significantly (p>0.05) lowered. Furthermore, there was an increase in MDA concentration but a decrease in SOD activity in the brain and serum of the experimental animals. Significance: Exposure to CaC2 induced adverse heamatobiochemical changes in rats which could signal danger to humans using this agent for fruit ripening.

Protective Effects of Luteolin and Gallic Acid Against Storage-Induced Oxidative Damage in Whole Blood of Female Wistar Rats

Introduction: Whole blood undergoes oxidative stress that precipitates biochemical changes that can lead to lesions during storage. This study attempts to evaluate the effectiveness of gallic acid and luteolin separately and in their combined state against oxidative damage during blood storage. Materials and Methods: Rats were grouped into control and experimental. Blood collected was stored for 28 days at 4°C. On day 0, 14, and 28, blood was withdrawn to study oxidative stress markers, antioxidant enzymes, and protein oxidation products. Results: Catalase activity reduced in all groups. Thiobarbituric acid reactive substance (TBARS) level increased in control without antioxidants (p < 0.05). Combined antioxidants or when separately added at lower concentrations, significantly reduced the TBARS level. Individual antioxidants at higher concentrations increased TBARS as compared with control (p < 0.05; p < 0.01). Decrease in superoxide dismutase activity observed in control was prevented by the antioxidants. Protein sulfhydryl level was restored and sustained until the last day of storage in groups that received individual antioxidants at both concentrations and the combined form at a lower concentration. Addition of either luteolin or gallic acid and their combined form reduced advanced oxidation protein products formation noticed in the control during storage. Conclusions: Luteolin and gallic acid were beneficial in the area of increased antioxidant capacity, prevention of protein product formation, and maintenance of sulfhydryl level. Their combination also showed a synergistic effect that offered a potential to improve long-term storage of whole blood. The antioxidants could possibly collaborate to be excellent potential blood storage additives providing protection against oxidative damage through their antiradical properties.

Turmeric and vitamin C mitigate testicular atrophy induced by lead diacetate via regulation of GRP-78/17β-HSD pathways in rat's model.

Occupational and ecological contacts to lead persist as a universal concern. Lead alters most of the physiological processes via enhancing oxidative stress. Thus, this study was purposed to assess the influence of turmeric (TMRC) and/or vitamin C (VIT-C) on Lead diacetate (Lead diAC)-induced testicular atrophy with an emphasis on oxidative stress, inflammation, BAX/STAR and GRP-78/17β-HSD signalling. Rats were injected with Lead diAC and then treated with TMRC and/or VIT-C orally for 1week. Lead diAC decreased serum testosterone and testicular glutathione levels. It also decreased superoxide dismutase activity. On the contrary, levels of malondialdehyde, tumour necrosis factor-α, IL-1β and caspase-3 were increased. mRNA levels and protein expressions of GRP-78 and BAX were upregulated, while the expression of both steroidogenic acute regulatory protein and 17β-HSD were downregulated. DNA fragmentation was increased as well. These changes were further confirmed by histopathological findings. Supplementation with TMRC and/or VIT-C ameliorated all of the above parameters. In Conclusion: TMRC or VIT-C specially in combination group prevents Lead diAC testicular damage via reduction of oxidative injury as well as inflammation, downregulation of GRP-78/BAX and upregulation of 17β-HSD and STAR expression as well as improvement in the histological architecture of the testis.

LncRNA OIP5-AS1 accelerates ox-LDL-treated HUVECs injury by NF-κB pathway via miR-30c-5p.

Oxidized low-density lipoprotein (ox-LDL) could induce endothelial injury and played a vital role in the progression and development of atherosclerosis. This study aimed to investigate the role of Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) in ox-LDL-induced human umbilical vascular endothelial cells (HUVECs) injury and the potential mechanisms. Cell proliferation and apoptosis were evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry assay, respectively. The levels of lactate dehydrogenase (LDH), reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were detected by corresponding detection kits, respectively. Quantitative real-time PCR (qRT-PCR) was conducted to measure the expression of OIP5-AS1 or microRNA-30c-5p (miR-30c-5p) in HUVECs. Binding between OIP5-AS1 and miR-30c-5p was predicted through bioinformatics analysis and confirmed by dual-luciferase reporter assay and RNA immunoprecipitation (RIP). Western blot was used to analyze p-IκB, IκB, p-p65 and p65 levels. In HUVECs, exposure to ox-LDL led to a decrease in cell viability and an increase in LDH release and apoptosis with concomitant enhancement of oxidative stress, as evidenced by increased ROS and MDA generation, as well as decreased SOD activity and NO levels, while OIP5-AS1 knockdown or miR-30c-5p upregulation could rescue these effects above. Mechanically, OIP5-AS1 functioned as a sponge of miR-30c-5p. OIP5-AS1-induced injury and apoptosis, oxidative stress and activation of NF-κB pathway were reversed by miR-30c-5p in ox-LDL-treated HUVECs. OIP5-AS1 contributed to ox-LDL-treated HUVECs injury by activation of NF-κB pathway via miR-30c-5p.

Mitochondrial dysfunction and potential mitochondrial protectant treatments in tendinopathy

Tendinopathy is a common musculoskeletal condition that affects a wide range of patients, including athletes, laborers, and older patients. Tendinopathy is often characterized by pain, swelling, and impaired performance and function. The etiology of tendinopathy is multifactorial, including both intrinsic and extrinsic mechanisms. Various treatment strategies have been described, but outcomes are often variable, as tendons have poor intrinsic healing potential compared with other tissues. Therefore, several novel targets for tendon regeneration have been identified and are being explored. Mitochondria are organelles that generate adenosine triphosphate, and they are considered to be the power generators of the cell. Recently, mitochondrial dysfunction verified by increased reactive oxygen species (ROS), decreased superoxide dismutase activity, cristae disorganization, and decreased number of mitochondria has been identified as a mechanism that may contribute to tendinopathy. This has provided new insights for studying tendinopathy pathogenesis and potential treatments via antioxidant, metabolic modulation, or ROS inhibition. In this review, we present the current understanding of mitochondrial dysfunction in tendinopathy. The review summarizes the potential mechanism by which mitochondrial dysfunction contributes to the development of tendinopathy, as well as the potential therapeutic benefits of mitochondrial protectants in the treatment of tendinopathy.

Diagnostic value of markers of oxidative stress and metabolic disorders in preterm infants in the early neonatal period

The aim of the study was to evaluate the markers of oxidative stress and metabolic disorders in preterm infants and to examine their association with short-term outcomes in the early neonatal period to identify the predictors of unfavourable outcome. The study included 46 preterm infants, gestational age ≤32 weeks, in the early neonatal period, i.e. group 1 of 12 infants with lethal outcome and group 2 of 34 preterm infants with favourable outcome. Markers of metabolic disorders, oxidative stress and antioxidant system were analysed in cord blood and urine on the first/second day of life. Evaluation of oxidative (8-isoprostane) and antioxidant system (catalase and superoxide dismutase (SOD) activity) and metabolic (lactate, pyruvate, lactate to pyruvate ratio (LPR), NAD+/NADH) stress parameters confirmed energy imbalance and presence of tissue hypoxia in preterm newborns with adverse outcomes. The following risk factors of unfavourable prognosis in preterm infants in the early neonatal period were identified: asphyxia (p=0.038), early-onset sepsis (p=0.003), intraventricular haemorrhage (p=0.029), hyperlactatemia (p=0.013), increased pyruvate level (p=0.002), increased LPR (p=0.008), decreased catalase (p=0.003) and SOD (p=0.001) activity. Logistic regression indicated that mortality rate was positively related to asphyxia, early-onset sepsis and lactate level, and negatively related to SOD activity. In conclusion, intensive oxidative and metabolic stress in preterm infants is associated with adverse outcomes in the early neonatal period. A combination of asphyxia and early-onset sepsis together with high lactate level and decreased SOD activity is a predictor of unfavourable out- come in the early neonatal period.

An isopentenyl transferase transgenic wheat isoline exhibits less seminal root growth impairment and a differential metabolite profile under Cd stress.

Cadmium is one of the most important contaminants and it induces severe plant growth restriction. In this study, we analyzed the metabolic changes associated with root growth restriction caused by cadmium in the early seminal root apex of wheat. Our study included two genotypes: the commercial variety ProINTA Federal (WT) and the PSARK ::IPT (IPT) line which exhibit high-grade yield performance under water deficit. Root tips of seedlings grown for 72 h without or with 10μM CdCl2 (Cd-WT and Cd-IPT) were compared. Root length reduction was more severe in Cd-WT than Cd-IPT. Cd decreased superoxide dismutase activity in both lines and increased catalase activity only in the WT. In Cd-IPT, ascorbate and guaiacol peroxidase activities raised compared to Cd-WT. The hormonal homeostasis was altered by the metal, with significant decreases in abscisic acid, jasmonic acid, 12-oxophytodienoic acid, gibberellins GA20, and GA7 levels. Increases in flavonoids and phenylamides were also found. Root growth impairment was not associated with a decrease in expansin (EXP) transcripts. On the contrary, TaEXPB8 expression increased in the WT treated by Cd. Our findings suggest that the line expressing the PSARK ::IPT construction increased the homeostatic range to cope with Cd stress, which is visible by a lesser reduction of the root elongation compared to WT plants. The decline of root growth produced by Cd was associated with hormonal imbalance at the root apex level. We hypothesize that activation of phenolic secondary metabolism could enhance antioxidant defenses and contribute to cell wall reinforcement to deal with Cd toxicity.

Ameliorating effect of melatonin against nicotine induced lung and heart toxicity in rats.

The present study was carried out to investigate the ameliorative effects of melatonin against nicotine-induced heart and lung toxicity. For this purpose, 75 mature male Sprague Dawley (SD) rats weighing 150-170 g were randomly divided into five groups (15 rats each): control group (rats were I/P injected with 1% ethanol in saline), nicotine group (rats were I/P injected with 0.6 mg/kg body weight), and combined nicotine and melatonin groups (rats received nicotine as in the previous group and melatonin at a dose of 1, 5, or 10 mg/kg body weight, respectively); all treatments were continued for 21 days. Fasting blood samples were collected from each rat at the 11th day and one day after the end of the last injection (22nd day) for complete blood count (CBC) determination, while sera were collected for the determination of lipid profiles. Malondialdehyde (MDA) concentration, superoxide dismutase (SOD) activity, and reduced glutathione (GSH) as well as DNA fragmentation percentage were assessed in cardiac tissue. Heart and lung samples were collected for estimation of caspase-3 expression and histopathological examination. The results revealed that nicotine increased the number of RBCs, Hb concentration, total cholesterol, and low density lipoprotein (LDL) and decreased high density lipoprotein (HDL). In addition, it decreased SOD activity and GSH concentration with increased MDA concentration, and DNA fragmentation in the heart, as well as caspase-3 expression in both heart and lungs. It also induced histopathological changes in the heart and lung tissues. Melatonin could ameliorate the deleterious effect of nicotine on the previous parameters either partially or completely, where melatonin restored complete blood count, improved lipid profile, mended lipid peroxidation and antioxidant parameters in the cardiac tissue, rectified caspase-3 expression in the heart and lungs, ameliorated DNA fragmentation percentage in the heart, and protected both heart and lung tissue against the harmful effect of nicotine. It is concluded that melatonin has a protective effect on the heart and lungs against the harmful effect of nicotine.

Sufentanil Affects High Glucose-Induced Oxidative Stress in and Apoptosis of Cardiomyocytes by Regulation of miR-142-3p Expression

To explore the effects and molecular mechanisms of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes, cardiomyocytes H9c2 cells were classified into groups based on different treatments as high-glucose (HG), HG with low, medium, or high-dose sufentanil, HG with high-dose sufentanil and anti-miR-NC, HG with high-dose sufentanil and anti-miR-142-3p, and control. The cells’ superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected using respective kits. The apoptosis rate in each group was detected by flow cytometry. The expressions of cleaved caspase-3 and pro-caspase3 were determined using western blotting. The expression of miR-142-3p in cardiomyocytes was detected using real-time fluorescent quantitative PCR. Compared with the control group, the HG group had decreased SOD activity, pro-caspase-3 expression, and miR-142-3p expression and increased MDA content, apoptosis, and cleaved caspase-3 expression (P &lt; 0.05). Compared with the HG group, the SOD activity and pro-caspase-3 expression increased and the MDA content, apoptosis rate, and cleaved caspase-3 expression decreased in HG cells treated with low, medium, or high-dose sufentanil. The expression of miR-142-3p was increased in a dose-dependent manner (P &lt; 0.05). The interference of miR-142-3p reversed the effect of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes. Sufentanil may inhibit high glucose-induced oxidative stress in and apoptosis of cardiomyocytes by upregulating miR-142-3p expression.

MiR-29a Alleviates High Glucose-induced Inflammation and Mitochondrial Dysfunction via Modulation of IL-6/STAT3 in Diabetic Cataracts

ABSTRACT Background: This in vitro study was designed to reveal the role of miR-29a in high glucose-induced cellular injury through the modulation of IL-6/STAT3 in diabetic cataracts. Methods: The expression of miR-29a and STAT3 in the lens capsules of patients with or without diabetes was determined by RT-PCR. The levels of the IL-6 proinflammatory cytokine in the aqueous humor were detected by ELISA. HLE B-3 cells were cultured in normal glucose (NG; 5 mM) or high glucose (HG; 40 mM). After transfection with miR-29a, si-STAT3, or a negative control vector, the levels of IL-6 and STAT3 were detected. A CCK-8 assay was used to determine cell viability. We used flow cytometry to assess changes in reactive oxygen species (ROS) production, mitochondrial membrane potential (MMP), and apoptosis induced by oxidative stress. Western blotting was used to determine the expression of the oxidative injury markers superoxide dismutase (SOD) and malondialdehyde (MDA) and the apoptosis markers Bcl-2 and Bax. Results: Reduced miR-29a, increased STAT3 expression, and IL-6 release were demonstrated in the lens capsules and aqueous humor of patients with diabetes. The stimulation of apoptosis and the loss of MMP induced by HG were attenuated by transfection with a miR-29a mimic and si-STAT3. ROS production, increased MDA content, decreased SOD activity, and upregulation of the apoptotic proteins Bcl-2/Bax were also partially alleviated by miR-29a overexpression, which shows their roles in oxidative injury. Furthermore, transfection with a STAT3 overexpression vector reversed the effects of miR-29a. Conclusions: In conclusion, miR-29a mitigated HG-induced oxidative injury and exerted protective effects via IL-6/STAT3 signaling. Thus, miR-29a may be a potential therapeutic agent for diabetic cataracts.

Коррекция α-токоферолом свободнорадикального дисбаланса крови и поведения пренатально стрессированных крыс

The research involved female mongrel white rats (n = 16) and their offspring (sexually mature males, n = 75). Pregnant females were divided into 4 groups: control (intact animals), stress (from the 16th to the 19th day of pregnancy females were subjected to 3-hour immobilization in plastic cases), stress+α-tocopherol (against the background of immobilization, females received α-tocopherol at a dose of 1 mg per 100 g of weight starting from the 2nd day of pregnancy), and α-tocopherol (females received α-tocopherol in the same dose and regimen as the group above). The control and stress groups received vegetable oil instead of α-tocopherol. In 3-month-old female offspring, we studied behaviour and determined the levels of products of free radical modification of proteins and lipids, total antioxidant activity as well as superoxide dismutase and ceruloplasmin activity in the blood plasma. Prenatal stress increased the exploratory and motor activity in offspring and modified the level of free radical homeostasis in the serum of male rats: there was an increase in the level of products of oxidative modification of proteins, thiobarbituric acid reactive substances concentration, end products of lipid peroxidation (Schiff bases), total antioxidant activity and ceruloplasmin activity, as well as a decrease in superoxide dismutase activity. Alpha-tocopherol taken by females during pregnancy brought all the oxidation parameters modified by immobilization to the values of the control group; the levels of primary products of oxidative modification of proteins and lipid peroxidation decreased two-fold, compared with the stress group. The activity of superoxide dismutase and ceruloplasmin returned to the control values, but the total antioxidant activity remained at the level of the stress group. Thus, there is reason to assume that α-tocopherol has a significant corrective effect on the intensity of free radical processes in prenatally stressed white male rats.

Neuroprotective Effect of Alkylresorcinols from Wheat Bran in HT22 Cells: Correlation with in vitro Antioxidant Activity

Alkylresorcinols (ARs), which are phenolic lipids found in wheat bran, have attracted a considerable amount of attention because of their antioxidant properties. However, the mechanism of ARs for regulating neuroprotective activity remains unclear. The correlation between the cellular neuroprotective effects of ARs in HT22 cells and their in vitro antioxidant activity were investigated. The results showed that two main constituents of crude ARs were C19:0 and C21:0, which was identified by high-performance liquid chromatography-atmospheric pressure chemical ionization tandem mass spectrometry. Pre-treatment with 400 μg/mL crude ARs could protect from H2O2-induced cellular damage involving low cell viability, leakage of lactate dehydrogenase and decreased superoxide dismutase activity. The maximum radical scavenging ability of DPPH•, ABTS•+, • and •OH– was 85.45%, 88.89%, 84.42% and 87.36%. The neuroprotection effect of ARs was significantly correlated with in vitro antioxidant capacity, confirmed by the maximum correlation coefficients being 0.9988, –0.9974 and 0.9972. The antioxidation of ARs potentially promoted neuroprotective effect and further study is needed to clarify the other mechanism behind ARs benefits.

THE ROLE OF QUALITY OF LIFE IN MELATONIN CONTENT AS A REGULATOR OF DEFENSE AND AGGRESSION FACTORS IN GASTROESOPHAGEAL REFLUX DISEASE PATIENTS WITH SLEEP APNEA SYNDROME

The aim of the study: to study the effect of the quality of life on the melatonin content, and at the same time to assess the state of the factors of aggression and protection of the esophageal mucosa in patients with GERD without comorbidities and with concomitant obstructive sleep apnea/hypopnea syndrome (OSAHS).&#x0D; Methods. 45 patients were taken for the study. 23 of them had GERD concomitant COPD, 22 were with isolated GERD with a non-erosive form.&#x0D; Melatonin levels were determined using the enzyme immunoassay method (ELIZA). Quality of life was assessed using the SF-36 questionnaire. Antioxidant protection of the mucous membrane (protection factor) – was assessed by the activity of superoxide dismutase (SOD). SOD activity in blood serum was determined by calorimetric method. Determination of the DC level was carried out in the blood by the spectrofluorimetric method.&#x0D; Results. The study showed that in patients with GERD with concomitant COPD, there is a significant decrease in the indicators of antioxidant activity and melatonin, both with indicators from the control group and with indicators of patients with GERD without comorbidity.&#x0D; At the same time, in patients with GERD without comorbidities, an increase in the level of DC was observed in comparison with the control group and patients with GERD with concomitant pathology and acidity of gastric juice.&#x0D; When analyzing the indicators of QOL in patients with GERD with concomitant pathology, there is a significantly more pronounced decrease in mental health, role emotional functioning and vitality.&#x0D; Conclusions. It has been established that in patients with GERD in the stage of exacerbation of the disease, there is a statistically significant decrease in QOL indicators with a high degree of reliability, manifesting itself in patients without combined pathology in the spectrum of indicators of the physical component of health, and in patients with GERD with concomitant obstructive sleep syndrome – in the spectrum of the psychological component quality of life.&#x0D; It has been shown that with a decrease in QOL in patients with GERD, the level of melatonin decreases, the decrease in which more clearly increases in patients with concomitant obstructive sleep apnea.&#x0D; Simultaneously with a drop in the level of melatonin in patients with GERD without associated pathology, the aggression factor increases with a high degree of certainty - that is, a decrease in the pH of gastric juice and an increase in the content of DC, while in patients with GERD with concomitant sleep apnea syndrome, the factor decreases with a high degree of certainty. Protection of the esophageal mucosa – (that is, a decrease in SOD activity), which must be taken into account when treating this category of patients.

Effects of Chronic Exposure to Low Levels of Dietary Aflatoxin B1 on Growth Performance, Apparent Total Tract Digestibility and Intestinal Health in Pigs.

Simple SummaryAflatoxin B1 (AFB1) is one of the most toxic mycotoxins compounds produced by Aspergillus, a common fungi contaminant in food and animal feed. Although there are many studies on AFB1, most of them are focused on the acute toxic effects of high-dose AFB1 ingestion. The symptoms of acute AFB1 mycotoxicosis are rarely observed in actual animal production. However, long-term exposure to low levels of AFB1 is common in swine production and may contribute to chronic diseases. Therefore, this study investigated the effects of chronic exposure to low levels of dietary AFB1 on growth performance, apparent total tract digestibility and intestinal health in pigs. We found that chronic exposure to low levels of dietary AFB1 suppressed growth performance, reduced apparent total tract digestibility and damaged intestinal barrier integrity in pigs, which could be associated with the decreased intestinal antioxidant capacity and the increased pro-inflammatory cytokine production. These results could provide new insights for future studies on the prevention and treatment of AFB1 poisoning.This study aimed to investigate the effects of chronic exposure to low levels of dietary aflatoxin B1 (AFB1) on growth performance, apparent total tract digestibility and intestinal health in pigs. In a 102-day experiment, fourteen barrows (Duroc×Landrace×Yorkshire, initial BW = 38.21 ± 0.45 kg) were randomly divided into control (CON, basal diet) and AFB1 groups (the basal diet supplemented with 280 μg/kg AFB1). Results revealed that the AFB1 exposure decreased the final BW, ADFI and ADG in pigs (p < 0.10). AFB1 exposure also decreased the apparent total tract digestibility of dry mater and gross energy at 50 to 75 kg and 105 to 135 kg stages, and decreased the apparent total tract digestibility of ether extract at 75 to 105 kg stage (p < 0.05). Meanwhile, AFB1 exposure increased serum diamine oxidase activity and reduced the mRNA abundance of sodium-glucose cotransporter 1, solute carrier family 7 member 1 and zonula occluden-1 in the jejunal mucosa (p < 0.05). Furthermore, AFB1 exposure decreased superoxide dismutase activity (p < 0.05) and increased 8-hydroxy-2′-deoxyguanosine content (p < 0.10) in jejunal mucosa. AFB1 exposure also increased tumor necrosis factor-α, interleukin-1β and transforming growth factor-β mRNA abundance in jejunal mucosa and upregulated Escherichia coli population in colon (p < 0.05). The data indicated that chronic exposure to low levels of dietary AFB1 suppressed growth performance, reduced the apparent total tract digestibility and damaged intestinal barrier integrity in pigs, which could be associated with the decreased intestinal antioxidant capacity and the increased pro-inflammatory cytokine production.

PREVENTIVE EFFECT OF PHASEOLUS VULGARIS SEED COATS ON PENTYLENETETRAZOLE (PTZ) INDUCED KINDLING AND BEHAVIORAL COMORBIDITIES

Introduction: To investigate the preventive effect of Phaseolus vulgaris seed coats on pentylenetetrazole-induced kindling and behavioral comorbidities. Material and Methods: Thirty Wistar albino rats were categorized into five groups. The first group received regular saline (0.9 % w/v NaCl) p.o.; the second group received PTZ (35 mg/kg b.w.) i.p.; the third group received valproic acid (200 mg/kg b.w.) p.o.; the fourth group received P. vulgaris extract (100 mg/kg b.w.) p.o.; the fifth group received P. vulgaris extract (200 mg/kg b.w.) p.o. on an alternate day for 21 days. PTZ improved lipid peroxidase levels, decreased Glutathione level, decreased superoxide dismutase activity, increased Nitric Oxide level. Result: This study revealed that P. vulgaris (Hydroalcoholic extract) increased the anti-oxidant level of both 100 mg/kg and 200 mg/kg compared to the PTZ category. Histopathological findings revealed that the hippocampal section of the brain of rats receiving P. vulgaris extract had improved relative to the receiving PTZ group. Conclusion: Based on the result, it is proposed that Phaseolus vulgaris has anti-oxidant properties. This is useful for the treatment of epilepsy.

Oxymatrine exerts a protective effect in myocardial ischemia/reperfusion‑induced acute lung injury by inhibiting autophagy in diabetic rats.

Oxymatrine (OMT) is the primary active component of Sophora flavescens Ait., and is widely used for the treatment of diabetic complications. The present study aimed to investigate the effects of OMT on acute lung injury (ALI) in diabetic rats subjected to myocardial ischemia/reperfusion (I/R). ALI in a myocardial I/R model was established in streptozocin-induced diabetic rats. Enzyme-linked immunosorbent assays were used to evaluate the levels of creatine kinase isoenzyme MB and lactate dehydrogenase, and the inflammatory response was assessed via leukocyte counts and the levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-8 in the bronchoalveolar lavage (BAL) fluid. Hematoxylin and eosin staining was used to determine pathological changes to the lung tissue, and the autophagy-related proteins LC-3II/LC-3I, Beclin-1, autophagy protein 5 (Atg5) and p62 were detected by western blotting. Diabetic rats subjected to myocardial I/R showed increased levels of ALI with a higher lung injury score and WET/DRY ratio, and lower partial pressure of oxygen. This was accompanied by aberrant autophagy, indicated by an increased LC-3II/LC-3I ratio, decreased p62 expression levels, increased Atg5 and beclin-1 expression levels, decreased superoxide dismutase activity and increased 15-F2t-isoprostane formation in lung tissues, as well as increased levels of leukocytes, TNF-α, IL-6 and IL-8 in the BAL fluid. Administration of the autophagy inducer rapamycin significantly accelerated these alterations, while the autophagy inhibitor 3-Methyladenine exerted the opposite effects. These results indicated that diabetic lungs are more vulnerable to myocardial I/R, which was associated with aberrant autophagy. Furthermore, oxymatrine was observed to reverse and alleviate ALI in diabetic rats with myocardial I/R in a concentration-dependent manner, the mechanism of which may be associated with the inhibition of autophagy.