Xanthine Oxidase Levels Research Articles

Lemon-Peel extract ameliorates rheumatoid arthritis by reducing xanthine oxidase and inflammatory cytokine levels

Abstract We investigated the effect of a lemon-peel extract in a rat model of rheumatoid arthritis and SW1353 chondrocytes. The rats were divided into control (sham), rheumatoid arthritis (control), extract (150 mg/kg bwt) and extract (300 mg/kg bwt) groups. Pyrogallic acid, caffeic acid, eugenol, p-coumaric acid, p‑hydroxyl benzoic acid, resorcinol, salicylic acid, luteoline, quercetin, chrysin, and luteolin-3‑methoxy‑7-rutinoside were noted in the extracts. The extract was administered orally for five consecutive weeks, and antioxidant and inflammatory markers were investigated. Extracts markedly increased the plasma levels of catalase, superoxide dismutase, reduced glutathione, glutathione peroxidase and zinc, and reduced those of lipid peroxidation, nitric oxide, uric acid, ceruloplasmin, copper, matrix metalloproteinase-3 and prostaglandin E2. Moreover, the extracts reduced the serum levels of interleukin-1 beta, tumor necrosis factor-alpha and interleukin-6. Extracts at 50, 100 and 150 mg/L reduced chondrocyte proliferation by 20.9, 38.8, and 52.1%, respectively, and reduced the reactive oxygen species and NF-κB levels by > 40%. Furthermore, the lemon-peel extract at 50, 100 and 150 mg/L reduced the xanthine oxidase level by 0.26-, 0.55- and 0.89-fold, respectively. Taking all these data together, it is suggested the lemon peel extract ameliorated rheumatoid arthritis, reduced the SW1353 chondrocyte proliferation, ROS, inflammatory cytokines, and xanthine oxidase levels.

Ginger (Zingiber officinale Roscoe) for the treatment and prevention of necrotizing enterocolitis

Ethnopharmacological relevanceNecrotizing enterocolitis (NEC) is the most important gastrointestinal emergency affecting especially preterm infants and causes severe morbidities and mortality. However, there is no cure. Oxidant stress, inflammation, apoptosis, as well as prematurity are believed to responsible in the pathogenesis of the disease. Ginger and its compounds have anti-inflammatory, antimicrobial, anti-oxidant properties and immunomodulatory, cytoprotective/regenerative actions. Aim of the studyThis study aimed to evaluate the beneficial effects of ginger on the intestinal damage in an experimental rat model of NEC. Materials and methodsThirty newborn Wistar rats were divided into three groups: NEC, NEC + ginger and control in this experimental study. NEC was induced by injection of intraperitoneal lipopolysaccharide, feeding with enteral formula, hypoxia-hyperoxia and cold stress exposure. The pups in the NEC + ginger group were orally administered ginger at a dose of 1000 mg/kg/day. Proximal colon and ileum were excised. Histopathological, immunohistochemical (TUNEL for apoptosis, caspase 3 and 8) and biochemical assays including xanthine oxidase (XO), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malonaldehyde (MDA) and myeloperoxidase (MPO), tumor necrosis factor-α (TNF-α), interleukin1β (IL-1β), and interleukin 6 (IL-6) activity were evaluated. ResultsCompared with the NEC group, the rat pups in the NEC + ginger group had better clinical disease scores and weight gain (p < 0.05). Macroscopic evaluation, Histopathologic and apoptosis assessment (TUNEL, caspase 3 and 8) releaved that severity of intestinal damage were significantly lower in the NEC + ginger group (p < 0.05). The levels of TNF-α, IL-1β and IL-6 in the ginger treated group were significantly decreased (P < 0.05). The GSH-Px and SOD levels of the ginger treated group were significantly preserved in the NEC + ginger group (p < 0.05). The tissue XO, MDA and MPO levels of the NEC + ginger group were significantly lower than those in the NEC group (P < 0.05). ConclusionGinger therapy efficiently ameliorated the severity of intestinal damage in NEC and may be a promising treatment option.

Silybum marianum provides cardioprotection and limits adverse remodeling post-myocardial infarction by mitigating oxidative stress and reactive fibrosis

AimsMilk thistle (Silybum marianum; SM) is an herb commonly used for hepatoprotection with antioxidant and antifibrotic properties. We investigated in pigs the cardiac effects of SM intake during the acute phase of myocardial infarction (MI) and remodeling period post-MI. MethodsStudy-1 tested the effect of SM use on the acute phase of MI. Hence, animals were distributed to a control group or to receive SM prior infarction (1.5 h ischemia). Animals were sacrificed after 2.5 h of reperfusion. Study-2 tested the effect of SM use in the cardiac remodeling phase. Accordingly, animals received for 10 d diet ± SM prior MI and followed the same regime for 3 weeks and then sacrificed. Study-3 tested the effect of SM in a non-infarcted heart; therefore, animals received for 10 d diet ± SM and then sacrificed. ResultsAnimals taking SM before MI showed a reduction in cardiac damage (decreased oxidative damage, ROS production and xanthine oxidase levels; preserved mitochondrial function; and increased myocardial salvage; p < 0.05) versus controls. Animals that remained on chronic SM intake post-MI improved left ventricular remodeling. This was associated with the attenuation of the TGFß1/TßRs/SMAD2/3 signaling, lower myofibroblast transdifferentiation and collagen content in the border zone (p < 0.05 vs. all other groups). Cardiac contractility improved in animals taking SM (p < 0.05 vs. post-MI-control). No changes in cardiac function or fibrosis were detected in animals on SM but without MI. ConclusionIntake of SM protects the heart against the deleterious effects of an MI and favors cardiac healing. These benefits may be attributed to the antioxidant and antifibrotic properties of SM.

Uric acid-lowering effect and intestinal permeability of Kampo medicine, Hachimijiogan, Yokuininto and Goshakusan

IntroductionThe aim of the present study was to investigate the uric acid-lowering effect of several Kampo (Japanese) herbal medicines (Hachimijiogan, Hangekobokuto, Yokuininto, Keishibukuryogan, Rikunshito, Kakkonto and Goshakusan), in a drug-permeability mimicked model using human intestinal epithelial Caco-2 cells. MethodsCaco-2 cells pretreated with potassium oxonate (PO) were treated with each medicine. The protein levels of xanthine oxidase (XO), glucose transporter 9 (GLUT9), and organic anion transporter 3 (OAT3) were determined via immunoblot analysis and ELISA. Caco-2 cell protein expression was additionally analyzed via immunofluorescence staining. OAT3 transporter uptake assays were measured by HEK293 cells overexpressing system. The levels of renal injury biomarkers, neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were measured. ResultsThe results indicated that Hachimijiogan, Yokuininto and Goshakusan upregulated OAT3 protein levels (18%, 35% and 34%, respectively) and downregulated GLUT9 protein levels (69%, 49% and 63%, respectively), reversing the effects of PO. In addition, they remarkably inhibited XO activity (40%, 45% and 36%, respectively) as well as inflammatory renal injury biomarkers, NGAL (32%, 51% and 52%, respectively) and KIM-1 protein levels (55%, 41% and 41%, respectively). The nominated herbal medicines can modulate the expression of OATs involved in uric acid uptake, and may have anti-inflammatory actions via the suppression of acute kidney injury biomarkers. ConclusionKampo medicines, Hachimijiogan, Yokuininto and Goshakusan were demonstrated to have anti-hyperuricemic effects by suppression of XO activity and regulation of uric acid transport proteins. Furthermore, Hachimijiogan, Yokuininto and Goshakusan were found to reduce the activities of NGAL and KIM-1.

Toxicities of selected medicinal plants and floras of lower phyla

The aim of this study was to evaluate the toxic effects associated with the administration of aqueous extracts (AE) of Calliandra portoricensis (CP), Dracaena arborea (DA), Duranta repens (DR), Polytrichum juniperinum (PJ), Parmelia caperata (PC), and Nostartium officinale (NO) on Wistar rats. LD50 for each plant was obtained prior to administration. Seven groups of six rats each were orally gavaged for 28 days as follows; group 1–7 received normal rat pellets and saline, in addition, group 2 received 20 mg/kg b.w CP, group 3 & 4 respectively received 8 mg/kg b.w DA and DR, group 5 & 6 respectively received 4 mg/kg b.w PJ and PC, and group 7 received 100 mg/kg b.w NO. Liver enzymes; ALP, ALT, AST and GGT were significantly (p < 0.05) elevated by CP, DR, PJ and PC extracts. All the extracts caused significant alterations of the total protein, albumin and globulin levels. The urea levels were deranged by all the extracts while CP, PJ, PC, and NO extracts caused no significant effects on the creatinine levels. Both DR and NO deranged the serum electrolytes; Na, K, Cl, and HCO3. Results for the lipid profile showed that all extracts significantly altered the phosphatidate phosphohydrolase and LDL levels while no significant effects were observed in the VLDL, TG, TC, HDL, cardiac risk ratio, arterogenic coefficients, and arterogenic index of plasma, of NO treated rats. For hematological parameters DR, PJ, and PC significantly deranged the RBC, HGB, MCHC, MCV, and MCH concentrations while the neutrophils, eosinophils and basophils were significantly altered on administration of all the extracts. No significant effects were observed on the platelets and plateletcrit level in rats gavaged with CP, whereas the MPV, PDW, and PCT concentrations were deranged by DR extracts. CP and NO caused no alterations in the MDA, GSH, and GST levels whereas the SOD, GPx, and xanthine oxidase levels were significantly deranged by all the plant extracts. Only NO treatment produced catalase, glutathione reductase, and xanthine dehydrogenase levels equivalent to the control group. This study has shown various degrees of deleterious effects on biochemical parameters associated with the consumption of these plants, thus raising serious concerns over their continuous applications as local medicaments.

Circulating cell-free DNA of methylated insulin-like growth factor-binding protein 7 predicts a poor prognosis in hepatitis B virus-associated hepatocellular carcinoma after hepatectomy

The initiation and progression of hepatocellular carcinoma (HCC) is a multistage process involving a variety of changes at the gene level. Methylation of insulin-like growth factor-binding protein 7 (IGFBP7) plays a crucial role in HCC development. The main purpose of this study was to investigate the relationship between oxidative stress, DNA methyltransferases (DNMTs) expression, and IGFBP7 methylation, and to evaluate the prognostic value of serum IGFBP7 methylation status in patients with HCC after hepatectomy. We enrolled 155 patients with HCC undergoing surgical resection. The IGFBP7 methylation status, DNMTs mRNA levels and malondialdehyde (MDA), xanthine oxidase (XOD), reduced glutathione hormone (GSH), and glutathione-S-transferases (GST) levels were detected. MDA and XOD levels were significantly higher in IGFBP7 methylated group than unmethylated group, while GSH level was lower in methylated group than unmethylated group. The DNMT1 and DNMT3a mRNA levels were higher in IGFBP7 methylated group than unmethylated group. Kaplan–Meier curve analysis revealed that IGFBP7 promoter methylation was significantly correlated with overall survival (OS) (p < .001). Moreover, IGFBP7 methylation was an independent prognostic predictor for OS (p = .000) and early tumour recurrence (ETR) (p = .008) in HCC after hepatectomy. Our results indicated that IGFBP7 promoter methylation was associated with oxidative stress and DNMTs expression. Meanwhile, IGFBP7 promoter methylation was associated with OS and ETR, indicating that it might serve as a potentially independent prognostic factor in patients with HCC after hepatectomy.

Detection of Xanthine Oxidase IN Breast Cancer

Thirty two females with breast cancer were studied .in this study xanthine oxidase levels were compared with normal females .Results obtained in the present study showed that high levels of xanthine oxidase in older age than in lower age . High level of xanthine oxidase was detected in patients having breast cancer and Diabetes Meilltus ,heart diseases, and anemia ,but no change in xanyhine oxidase was detected in breast cancer with hyperytension . key words: xanthine oxidase ,breast cancer.Breast cancer is a type of cancer originating from breast tissues, most commonly from the inner lining of milk ducts or the lobules that supply the ducts with milk(1).The size, stage, rate of growth and other characteristic determine the kind of treatment (2.) Breast cancer may be invasive or noninvasive. Invasive means it has spread from the milk duct or lobule to other tissues in the breast. Noninvasive means it has not yet invaded other breast tissue(3). Xanthine oxidase (XO) is the final enzyme in the degradation of purines. It converts hypoxanthine to xanthine and subsequently to uric acid. Unlike other oxidases. lmmunohistochemical location of XO has been reported its presence in various tissues from various animal species( 4) .Other researcher demonstrated the ubiquitous localization of this cytosolic enzyme in human tissues, such as tongue,esophagus, trachea, sweat glands, mammary glands, small and large intestine, renal tubules skeletal muscle, lung, spleen and liver. It was found that human blood or serum contains XO activity, since high concentration of XO antibodies are present in human sera (5).XO may play a beneficial role by producing superoxide radicals (6). Previous studies suggested a role of XO as an antimicrobial agent (7).. Moreover, it was reported that uric acid, in its normal range,serve as an antioxidant. Therefore, XO serves as a defense mechanism by generating uric acid as well(6).This study was conducted in Iraqi center for cancer research and medical genetic. Thirty two With age range 40-73 years, had breast cancer diagnosed by history, clinical and laboratory findings, and twenty controls with range age 30-75 years old, had no evidence of diseases of diseases. Blood was collected from a forearm vein.Blood samples were allowed to clot at room temperature and serum was separated by centerfugation at 1500g for 10 min. Xanthine Oxidase Assay: Xanthine Oxidase(XO,EC 1.17.3.2). In this assay XO oxidizes xanthine to hydrogen peroxide which reacts with stoichiometrically with OxiRedTM probe to generate color( at lambda=570nm).Since the color intensity is proportional to XO cotent,the XO activity can be accurately measured. 1-Standard curve preparations: It has been added 0, 10, 20 , 30 , 40 , 50 ul of the 0.1mM H2O2 standard,to generate 0 ,1 ,2 ,3 ,4 ,5 nmol/ well H2O2 standard. 2- Sample preparation: 44 ul buffer , 2ul substrate, ,2 ul enzyme mix , 2ul probr. 3-It has been measured the plate immediately (O,D=570 nm) for colorimetric assay. 4 – XO activity = B/(T2-T1Xv) x Sample Dilution Factor = nmol / min/ml = mU/ml Where; B is the amount of H2O2 Generated by XO from standard curve(in nmol). T1 is the time of first reading(A1) (in min ) T2 is the time of second reading (A2)(in min) V is the pretreated sample volume added into the reaction well (in ml ).

Curcumin ameliorated ventilator-induced lung injury in rats

BackgroundCurcumin (CUR) is a Chinese medicine monomer with antioxidant and anti-inflammatory properties. The aim of this study was to investigate the effects and mechanisms of CUR treatment on ventilator-induced lung injury (VILI) in rats. MethodsTotal 50 SD rats were divided into five groups: sham, VILI, VILI+CUR-50 (CUR 50 mg/kg pretreated intraperitoneal), VILI+CUR-200 (CUR 200 mg/kg pretreated intraperitoneal) and VILI + DXM (5 mg/kg pretreated intraperitoneal). The morphology and ultrastructure were observed by microscope and transmission electron microscope. The wet to dry ratio, protein concentration in bronchoalveolar lavage fluid (BALF), evans blue dye (EBD) content, nuclear factor kappa B (NF-κB) activity, myeloperoxidase (MPO), malondialdehyde (MDA), xanthine oxidase (XO) and total antioxidative capacity (TAOC) levels were measured. ResultsHistological studies revealed that inflammatory cells infiltration and alveolar edema were significantly severe in VILI as compared to other groups. CUR-200 and DXM treatment reversed lung injury significantly. The wet to dry ratio, protein concentration in BALF, EBD content, MPO activity, tumor necrosis factor (TNF)-α level and NF-κB activity were significantly increased in VILI group as compared to other groups. CUR-200 and DXM treatment significantly suppressed permeability and inflammation induced by ventilation. Furthermore, the significantly higher MDA content in VILI could be markedly decreased by CUR-200 and DXM treatment while the levels of XO and TAOC were markedly recovered only by CUR (200 mg/kg) treatment after VILI. ConclusionCUR could inhibit the inflammatory response and oxidative stress during VILI, which is partly through NF-κB pathway.

FISH OIL AND OXIDATIVE STRESS IN CHILDREN WITH GROWTH DELAY

Ponte Academic JournalNov 2018, Volume 74, Issue 11 FISH OIL AND OXIDATIVE STRESS IN CHILDREN WITH GROWTH DELAYAuthor(s): Zahide Yalaki ,Bilal Aytac, Bulent Alioglu, M. Aysin Tasar, Esra Durak, Tugba Zengin, Inci Arikan, Ilker DurakJ. Ponte - Nov 2018 - Volume 74 - Issue 11 doi: 10.21506/j.ponte.2018.11.9 Abstract:Aim: Oxidative stress results from an imbalance between antioxidant enzymes and various oxidants. The aim of this study was to evaluate how the effect of omega-3 on oxidants and antioxidants may support development in children with borderline growth delay. Population and Methods: 26 children with borderline growth delay were the patient group (between 2 and 9.5 years of age) and 30 healthy children with normal development were the control group. Patient group were given fish oil treatment for 4-weeks. All oxidant/antioxidant parameters were analyzed before and after treatment. Results: Prior to fish oil treatment, the levels of catalase antioxidants in the patient group were higher than those in the control group (p=0.013) while glutathione peroxidase levels were lower (p=0.0001). There were no differences in levels of xanthine oxidase and nitric oxide oxidants; malondialdehyde and nitric oxide synthase levels were higher (p=0.002; p=0.0001) compared to the control group prior to treatment. A decrease in catalase and an increase in glutathione peroxidase levels were detected in the patient group subsequent to the fish oil treatment. Xanthine oxidase levels increased (p=0.031) while malondialdehyde levels fell with treatment compared to the control group. Patient group’s glutathione peroxidase levels also increased following treatment (p=0.0001) while a significant decrease was observed in oxidant of nitric oxide synthase levels (p=0.002). Conclusions: The use of fish oil supplementation was observed to contribute effectively to a reduction in oxidant stress while, at the same time, recovering antioxidant balance. Download full text:Check if you have access through your login credentials or your institution Username Password

Alpinetin improved high fat diet-induced non-alcoholic fatty liver disease (NAFLD) through improving oxidative stress, inflammatory response and lipid metabolism

The non-alcoholic fatty liver disease (NAFLD) has become a serious medical problem and an increasing threat to public health. It is characterized by the abnormal fat accumulation in liver without excessive alcohol intake. The concurrent NAFLD might up-regulate the risk of chronic kidney disease as well as the mortality rate. Though various drugs have been investigated to attenuate NAFLD, further study is still necessary to find new therapeutic strategy and to reveal the underlying molecular mechanism. In the present study, NAFLD animal models were induced by feeding with high fat (HF) diet for 8 weeks. Alpinetin (ALP) was given to mice for another 8 weeks together with HF. Hepatic and renal function, oxidative stress, inflammatory response and lipid metabolism were calculated. And human liver cells of HL-7702 were cultured with high fructose (5mM) with or without ALP. The findings indicated that ALP down-regulated lipid accumulation in liver tissue samples. The higher inflammatory score induced by HF in liver and renal were reduced by ALP. HF-triggered oxidative stress was inhibited in ALP-treated groups, as evidenced by enhanced SOD1/HO-1/Nrf-2 expressions and reduced thioredoxin-interacting protein (TXNIP)/xanthine oxidase (XO) levels. ALP also suppressed inflammatory response by decreasing pro-inflammatory cytokines through inactivating toll-like receptor 4-nuclear factor kappa B (TLR4-NF-κB) pathway. The anti-oxidant and anti-inflammatory effects of ALP were confirmed in HL-7702 cells. Further, abnormal lipid metabolism caused by HF was alleviated by ALP, which was associated with the decreased Stearoyl-CoA desaturase 1 (SCD1), fatty acid synthase (FAS), sterol element regulatory binding protein 1c (SREBP-1c), Liver X Receptor (LXR)-α, elongases of very long-chain fatty acids (Elovl)-2, p-insulin receptor substrate 1 (IRS1) expressions, and increased PPARα levels. Taken together, the results above indicated that ALP could suppress oxidative stress, reduce inflammatory response and attenuate lipid metabolism, preventing NAFLD.

Effects of acupuncture at Shu, Yuan, and Mu acupoints on blood serum uric acid and xanthine oxidase levels in a rat model of gout and hyperuricemia

ObjectiveTo investigate the effects of needling the Shu, Yuan, and Mu acupoints on serum uric acid (SUA), xanthine oxidase (XOD), and alkaline phosphatase (ALP) levels and the kidney index in a rat model of gout and hyperuricemia. MethodsFifty rats were randomly divided into five groups: blank, model, Shu-acupoint, Yuan-acupoint, and Mu-acupoint groups. A rat model of hyperuricemia was developed by intragastric administration of adenine and ethambutol. This experiment last for 90 d in total. Treatment groups underwent 3 courses of acupuncture. Each course involved a total of 10 interventions (one intervention every second day) with each intervention lasting 15 min. There was a break for 10 d between courses. SUA and ALP were analyzed using an automatic biochemical analyzer and XOD was analyzed using immunofluorescence. ResultsCompared with the blank group, SUA and XOD levels in the model group were significantly higher and the renal index significantly improved. Compared with the model group, SUA and XOD levels in the three treatment groups decreased and the renal index significantly improved. When the three treatment groups were compared, the Mu-acupoint group showed the greatest decreases in SUA and XOD levels, followed by the Yuan-acupoint group. There was no significant difference in kidney index among the three treatment groups. There was no significant difference in ALP levels among the groups. ConclusionThe three treatments showed significantly reduced SUA and XOD levels compared with the control groups, possibly suggesting reduced renal damage.

The oxidative/anti-oxidative effects of sevoflurane on reproductive system of females: An experimental study.

Objective:A permanent balance exists between the production and elimination of reactive oxygen species in all living organisms. The aim of this study was to evaluate the effects of sevoflurane possibly causing an imbalance in the equation of reactive oxygen species on the female rat reproductive system.Materials and Methods:A total of 30 adult female Wistar-albino rats were placed into an anesthesia chamber to administer sevoflurane. Rats were randomly divided into six groups, each group consisting of five rats: the control group received 2 L/min O2 18 min/day for seven days; the first group received 1 minimum alveolar concentration (MAC) of sevoflurane and 2 L/min O2 18 min/day for seven days; the second group received 1 MAC of sevoflurane and 2 L/min O2 18 min/day for seven days with no treatment for the next seven days; the third group received 1 MAC of sevoflurane and 2 L/min O2 18 min/day for 14 days; the fourth group received 1 MAC of sevoflurane and 2 L/min O2 18 min/day for 14 days with no treatment for the next seven days; and the fifth group received 1 MAC of sevoflurane and 2 L/min O2 18 min/day for 14 days with no treatment for the next 14 days. Bilateral ovaries were subsequently removed for biochemical analysis of tissue anti-oxidative enzyme levels.Results:Slight fluctuations were detected in mean nitric oxide, prostaglandin E2, prostaglandin F2-alpha, superoxide dismutase, glutathione peroxidase, malondialdehyde, alginate dialdehyde, and xanthine oxidase levels between the groups; however, the differences were not significant (p>0.05).Conclusion:Sevoflurane has no effect on the activity of anti-oxidant systems in the rat ovary.

Budesonide instillation immediately after reperfusion ameliorates ischemia/reperfusion-induced injury in the transplanted lung of rat

ABSTRACT Purpose: Lung ischemia-reperfusion injury (LIRI) after lung transplantation can lead to primary graft dysfunction. Budesonide can improve endothelial function to reduce lung injury. This study was aimed to examine the effects of budesonide on LIRI and potential mechanisms. Methods: Wistar rats were randomized and transplanted with syngeneic left lung or received the sham surgery. The recipients were instilled with saline or budesonide immediately after reperfusion. The mean arterial pressure (MAP), blood gas, and lung histology were analyzed. The ratios of wet to dry lung weights, the levels of total proteins, tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-6, and IL-10, and neutrophil elastase in bronchoalveolar lavage fluid (BALF) were measured. The levels of malondialdehyde (MDA), myeloperoxidase (MPO), and xanthine oxidase (XO) in the lung, and the levels of plasma lymphocyte function-associated antigen (LFA)-1 and P-selectin were determined. Results: Compared with the saline group, treatment with budesonide significantly increased blood PaO2, but reduced PaCO2, and mitigated lung damages after reperfusion, the levels of BALF proteins, and the ratios of wet to dry lung weights in rats. Furthermore, treatment with budesonide significantly decreased the levels of MDA, MPO, and XO in the lung and the levels of TNF-α, IL-1β, IL-6, and neutrophil elastase, but increased IL-10 in the BALF, accompanied by significantly reduced levels of serum P-selectin and LFA-1 in rats. Conclusions: Budesonide effectively mitigated LIRI and ameliorated the lung function by attenuating oxidative stress and inflammation following syngeneic lung transplantation.

Gebe Ratlara uygulanan Akrilamid ve E Vitaminin Plasenta Dokusu Üzerine Olası Etkilerinin Araştırılması

Investigate the changes that occur in the placenta tissues of pregnant rats that were administered acrylamide (AA) and vitamin E as a protective agent during pregnancy.&#x0D; Thirty rats that were proven positive for pregnancy with vaginal smear test were randomly distributed into control, corn oil, vitamin E, acrylamide and vitamin E + acrylamide groups. Pregnant rats were decapitated on the 20th day of the experiment. Malondialdehyde (MDA), reduced glutathione (GSH), total antioxidant capacity (TAS), total oxidant capacity (TOS) and Xanthine oxidase (XO) levels were measured in placenta tissues. It was determined that acrylamide application during pregnancy statistically significantly increased MDA, TOS and XO levels and reduced GSH and TAS levels in the placenta tissue of pregnant rats when compared to all other groups, and GAS and TAS levels statistically significantly increased in vitamin E administered group when compared to all other groups and TOS and XO levels were decreased to control group levels. It was observed that orally administered AA changed the antioxidant / oxidant equilibrium favoring the oxidants by increasing MDA, XO and TOS levels in pregnant rats and caused oxidative stress, while vitamin E administration returned the antioxidant / oxidant equilibrium back to normal levels, preventing oxidative stress induced toxicity.

Gypenosides Inhibits Xanthine Oxidoreductase and Ameliorates Urate Excretion in Hyperuricemic Rats Induced by High Cholesterol and High Fat Food (Lipid Emulsion).

BackgroundThe aim of this study was to study the effects of gypenosides (GPS) on lowering uric acid (UA) levels in hyperuricemic rats induced by lipid emulsion (LE) and the related mechanisms. GPS are natural saponins extracted from Gynostemma pentaphyllum.Material/MethodsForty-eight male SD rats were randomly divided into six groups: normal, model, two positive controls, and two GPS treated groups (two different doses of GPS). The normal group rats were fed a basic diet, and the other rats were orally pretreated with LE. Urine and blood were collected at regular intervals. Full automatic biochemical analyzer was used to detect the concentration levels of serum UA (SUA), serum creatinine (SCr), BUN, and urine UA (UUA), and urine creatinine (UCr) and fractional excretion of UA (FEUA). ELISA kits were used to detect enzymes activities: xanthine oxidase (XOD), adenosime deaminase (ADA), guanine deaminase (GDA), and xanthine dehydrogenase (XDH). Immunohistochemistry was used to observe kidney changes and protein (URAT1, GLUT9, and OAT1) expression levels. RT-PCR was used to detect the relevant mRNA expression levels.ResultsTreatment with GPS significantly reduced the SUA, prevented abnormal weight loss caused by LE, and improved kidney pathomorphology. Treatment with GPS also decreased the levels of XOD, ADA, and XDH expression, increased the kidney index and FEUA, downregulated URAT1 and GLUT9 expression and upregulated OAT1 expression in the kidney.ConclusionsGPS may be an effective treatment for hyperuricemia via a decrease in xanthine oxidoreductase through the XOD/XDH system; and via an increase in urate excretion through regulating URAT1, GLUT9, and OAT1 transporters.

Hepatic xanthine oxidase activity and purine nucleosides levels as physiological mediators to analyze a subcutaneous treatment with (PhSe)2 in mice infected by Toxoplasma gondii.

The aim of this study was to evaluate the levels of purine nucleosides and xanthine oxidase (XO) activity in the liver of mice chronically infected by Toxoplasma gondii and treated with diphenyl diselenide (PhSe)2. For this experiment, forty Swiss mice were used. Twenty animals were orally infected by approximately 50 bradizoites of a cystogenic ME-49 strain of T.gondii, and the same number of uninfected mice was used as a control group. Ten infected and ten uninfected mice were subcutaneously treated twice (days 1 and 20 post-infection (PI)) with 5μmolkg-1 of (PhSe)2. On day 30 PI, liver samples were collected to measure the levels of hypoxanthine (HYPO), xanthine (XAN), uric acid (UA), and XO activity. Infected animals showed increased (P<0.05) levels of hepatic XAN and UA, as well as XO activity compared to uninfected animals. The use of (PhSe)2 in healthy mice increased the levels of all nucleosides, but decreased XO activity compared to healthy untreated animals. The group of infected and treated animals showed increased XAN and UA levels, and XO activity compared to the healthy control group, however infected and treated mice showed a decrease in the XO activity compared to the infected untreated group. We conclude that chronic infection caused by T.gondii can induce hepatic changes, such as increased UA levels and XO activity, that can increase the pro-oxidative profile. The (PhSe)2 treatment of healthy animals altered the levels of nucleosides, possibly due to low XO activity that decreased nucleoside degradation. Finally, (PhSe)2 treatment decreased XO activity in the infected group and increased nucleoside levels; however it was unable to reduce the UA levels found during the infection.

Anti-Gouty Arthritis and Antihyperuricemia Effects of Sunflower (Helianthus annuus) Head Extract in Gouty and Hyperuricemia Animal Models.

This study was performed to investigate the therapeutic effects and possible mechanisms of sunflower (Helianthus annuus) head extract (SHE) on gout. First, the components of sunflower head powder and SHE were analyzed systematically. SHE, especially SHEB (extracted with 20% ethanol and 80% double-distilled water), strongly suppressed the swelling of the ankles in rats with acute gout induced by monosodium urate (MSU) crystals and reduced the levels of uric acid and xanthine oxidase (XO) in mice with hyperuricemia induced by oteracil potassium and yeast extract powder. Hematoxylin and eosin staining indicated that SHEB reduced inflammation cells and increased the joint space in the ankle compared with the control rats with MSU-induced gout. In the rats with acute gout, among 13 detected inflammatory cytokines, SHEB significantly enhanced the serum levels of interleukin-10 and the monocyte chemoattractant protein 1α. In the mice with hyperuricemia, SHEB reduced the levels of glutathione peroxidase, superoxide dismutase, malondialdehyde, and nitrogen monoxide in liver tissues. The potential therapeutic effects of SHE on gout are probably due to the production of anti-inflammatory cytokines and the suppression of XO activity via the modulation of oxidative stress status.

Chronic alcohol administration affects purine nucleotide catabolism in vivo

AimsTo investigate the relationship between chronic alcohol administration and purine nucleotide metabolism in vivo. Main methodsRat models of alcohol dependence and withdrawal were used. The concentrations of uric acid (UAC), urea nitrogen (UREA), creatinine (CREA), and beta-2-microglobulin (β2-M) and creatinine clearance rate (CCR) in plasma were measured. The PLC method was used to detect the absolute content of purine nucleotides in different tissues. Enzymatic activities of adenosine deaminase (ADA), xanthine oxidase (XO), ribose 5-phosphate pyrophosphokinase (RPPPK), glutamine phosphoribosylpyrophosphate amidotransferase (GPRPPAT), hypoxanthine-guanine phosphate ribose transferase (HGPRT), and adenine phosphoribosyltransferase (APRT) in the tissues were analyzed. Real-time PCR was used to determine the relative level of ADA and XO. Key findingsThe renal function of rats with alcohol dependence was normal. Further, the content of purine nucleotides (GMP, AMP, GTP, and ATP) in tissues of the rats was decreased, which indicated that the increased uric acid should be derived from the decomposition of nucleotides in vivo. The activity of XO and ADA increased, and their mRNA expression was enhanced in the alcohol dependence group, but there was no significant difference in the activity of RPPPK and GPRPPAT in the liver, small intestine, and muscle; furthermore, no significant difference in the activity of HGPRT and APRT was observed in the brain. SignificanceThese results indicate that chronic alcohol administration might enhance the catabolism of purine nucleotides in tissues by inducing gene expression of ADA and XO, leading to elevation of plasma uric acid levels.

Preconditioning with Azadirachta indica ameliorates cardiorenal dysfunction through reduction in oxidative stress and extracellular signal regulated protein kinase signalling

BackgroundAzadirachta indica is widely distributed in Africa, Asia and other tropical parts of the world. A. indica (AI) is traditionally used for the treatment of several conditions including cancer, hypertension, heart diseases and skin disorders. Intestinal ischaemia-reperfusion is a common pathway for many diseases and may lead to multiple organ dysfunction syndrome and death. ObjectiveIn this study, we investigated the ameliorative effects of AI on intestinal ischaemia-reperfusion injury-induced cardiorenal dysfunction. Materials and methodsSixty rats were divided into 6 groups; each containing 10. Corn oil was orally administered to group A (control) rats for 7 days without intestinal ischaemia-reperfusion injury. Group B underwent intestinal ischaemia-reperfusion injury (IIRI) without any pre-treatment. Groups C, D, E and F were pre-treated orally for 7 days with 100 mg/kg AI (100 and (200 mg/kg) vitamin C (100 and 200 mg/kg) respectively and thereafter underwent IIRI on the 8th day. ResultsThe cardiac and renal hydrogen peroxide increased significantly whereas serum xanthine oxidase and myeloperoxidase levels were significantly elevated (p < 0.05) in IIRI only when compared to the control. The cardiac and renal reduced glutathione, glutathione peroxidase, protein thiol, non-protein thiol and serum nitric oxide (NO) decreased (p < 0.05) significantly following IIRI. Immunohistochemical evaluation of cardiac and renal tissues showed reduced expressions of the extracellular signal regulated kinase (ERK1/2) in rats with IIRI only. However, pre-treatment with A. indica and vitamin C significantly reduced markers of oxidative stress and inflammation together with improvement in antioxidant status. Also, reduced serum NO level was normalised in rats pre-treated with A. indica and vitamin C with concomitant higher expressions of cardiac and renal ERK1/2. ConclusionsTogether, A. indica and vitamin C prevented IRI-induced cardiorenal dysfunction via reduction in oxidative stress, improvement in antioxidant defence system and increase in the ERK1/2 expressions. Therefore, A. indica can be a useful chemopreventive agent in the prevention and treatment of conditions associated with intestinal ischaemia-reperfusion injury.

Relationship Between Xanthine Oxidase, Ischemia Modified Albumin, Nitric Oxide with Antioxidants in Non Pregnants, Pre and Post-delivery of Normal Pregnants and Preeclampsia.

Preeclampsia is a multisystem disorder involves altered homeostasis of oxidants-antioxidants, inflammatory process and endothelial dysfunction. The present study aim was to determine the levels of oxidative stress parameters (malondialdehyde, protein carbonyl, ischemia modified albumin and xanthine oxidase), nutrient antioxidants (vitamin C and vitamin E), enzyme antioxidants (catalase, superoxide dismutase, glutathione peroxidase glutathione reductase), total antioxidant status (TAS) and its association with nitric oxide. The study population consists of three groups, non pregnants (Group 1, n=57), normotensive pregnants (Group 2, n=57) and Preeclampsia (Group 3, n=57). Group 2 and 3 were followed after delivery within 48h. In preeclampsia xanthine oxidase, malondialdehyde and uric acid levels were significantly increased (p<0.001), while TAS decreased (p<0.05) when compared to normotensive pregnant and non pregnant. Catalase, glutathione reductase levels were increased (p<0.005) and vitamin E, super oxide dismutase levels were decreased (p<0.001) in preeclampsia when compared to normal pregnants. Receiver operating characteristics curve analysis showed area under curve for xanthine oxidase (0.8), malondialdehyde (0.804), Uric acid (0.84), ischemia modified albumin (0.92) and catalase (0.88) which indicated as good markers in preeclampsia. Amongst, ischemia modified albumin is a better marker of intrauterine hypoxic reperfusion risk with sensitivity 87.7% and specificity 91.2%. The increased hydrogen peroxide from xanthine oxidase adds to oxidative stress and increased catalase activity in preeclampsia represents combating action. Increased oxidative stress, decreased TAS and its apparent reversible changes evinced within 48h after delivery in preeclampsia illustrated that placental abnormality is the contributing factor in the pathogenesis.