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Chronic alcohol consumption is associated with progressive/irreversible neurodegeneration. However, there is not a clear understanding of its discrete pathophysiology or therapeutic intervention. The present study aimed to investigate the protective effect of the natural citrus flavonoid, naringenin (NAG), against alcohol-induced neurodegeneration in the brain cerebral cortex. Thirty-two male albino rats were randomly divided into four equal groups (eight rats each): control group (I); NAG-treated group (II); alcohol-intoxicated group (III) and alcohol + NAG co-treated group (IV). Brain nuclear factor erythroid 2-related factor 2 and receptor-interacting protein kinase 3 expression were assessed by real-time polymerase chain reaction. NAD(P)H quinone oxidoreductase 1 activity and malondialdehyde, reduced glutathione, mixed lineage kinase-like protein, phosphorylated glycogen synthase kinase 3 beta, and ciliary neurotrophic factor levels were all measured biochemically. B-cell lymphoma 2 expression was assessed by immunohistochemistry. A histopathological examination and neurobehavioral tests were performed. The alcohol-treated group showed a significant increase in oxidative stress and necroptosis biomarkers with a significant reduction in neuroprotective proteins. NAG co-administration effectively ameliorated cognitive dysfunction with an apparent neuroprotective effect by targeting various signaling pathways, including nuclear factor erythroid 2-related factor/NAD(P)H quinone oxidoreductase 1, anti-oxidant capacity, attenuated necroptosis, and upregulated neuroprotective ciliary neurotrophic factor. The study findings suggest NAG as a possible management strategy for alcohol-induced neurodegeneration.

Prolonged dexamethasone (DEX) administration causes skeletal muscle atrophy through induction of both oxidative stress and mitochondrial dysfunction. Lipoxin A4 (LXA4) is a recognized antioxidant but its effect against DEX-induced muscle atrophy has not been studied yet. This study aimed to assess the potential ameliorating effect of LXA4 on DEX-induced muscle atrophy and investigate the possible involvement of the mitochondrial dynamics pathway and the redox state in this effect. Forty male rats were divided into four groups; normal control, LXA4-treated, DEX-treated, and LXA4 plus DEX-treated. At the end of the experiment, LXA4 counteracted the effect of DEX on different parameters including muscle weight, muscle strength, serum creatine kinase activity, malondialdehyde and protein carbonyl contents, Na/K-ATPase and citrate synthase activities, mitochondrial transmembrane potential, mitochondrial transcription factor (TFAM), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and nuclear factor erythroid 2-related factor 2 (Nrf2). These findings signify the promising therapeutic effect of LXA4 against DEX-induced skeletal muscle atrophy and indicate the possible involvement of LXA4-induced mitochondrial activation in addition to its well-known antioxidant effects.

The prevalence of obesity and its associated metabolic disorders, along with their healthcare costs, is rising exponentially. Irisin, an adipomyokine, may serve as a critical cross-organ messenger, linking skeletal muscle with adipose tissue and the liver to integrate the energy homeostasis under diet-induced obesity. We aimed to explore the putative role of irisin in the protection against obesity in a postmenopausal rat model by modulating energy expenditure (EE). Bilateral ovariectomy (OVX) was performed. After 3 weeks of recovery, the OVX rats were classified according to their dietary protocol into rats maintained on normal diets (ND) (OVX) or high-fat diet (HFD) groups. The HFD-fed animals were equally divided into OVX/HFD, or irisin-treated OVX/HFD groups. Sham rats, maintained on ND, were selected as the control group. We evaluated anthropometric, EE, and molecular biomarkers of browning and thermogenesis in inguinal white adipose tissue and skeletal muscle, and the activity of the proteins related to mitochondrial long chain fatty acid transport, oxidation, and glycolysis. HFD of OVX further deteriorated the disturbed glucose homeostasis, lipid profile, and the reduced irisin, thermogenic parameters in adipose tissue and skeletal muscle, and EE. Irisin treatment improved the lipid profile and insulin resistance. That was associated with reduced hepatic gluconeogenic enzyme activities and restored hepatic glycogen content. Irisin reduced ectopic lipid infiltration. Irisin augmented EE by activating non-shivering thermogenesis in muscle and adipose tissues and decreasing metabolic efficiency. Our experimental evidence suggests irisin’s use as a potential thermogenic agent, therapeutically targeting obesity in postmenopausal patients. Graphical abstract Irisin modulates the non-shivering thermogenesis in skeletal muscle and adipose tissue in postmenopausal model

Aim of the work To assess serum interleukin-6 (IL-6) level in primary fibromyalgia syndrome (FMS) patients and to study its relation to disease burden parameters Patients and methods Forty primary FMS patients and 40 age and sex matched controls were studied. Patients answered multiple questionnaires. Fatigue was assessed by multidimensional fatigue inventory (MFI-20), pain severity by visual analogue scale (VAS-pain) and sleep quality by sleep quality numerical rating scale (NRS). The 36-Item Short Form (SF-36) was used to assess quality of life and fibromyalgia Impact Questionnaire (FIQ) was used to evaluate patient status, progress and outcomes. Results The patients mean age was 36.5 ± 7.1 years and disease duration 5.3 ± 2.95 years and they were 38 females and 2 males. The mean serum IL-6 level was significantly higher in patients (134.9 ± 67.3 pg/ml) than control (41.1 ± 8.5 pg/ml)(p = 0.001). The mean VAS-pain was 6.2 ± 1.3 (4–8), FIQ was 58 ± 6.1 (50–70), SF-36 47 ± 10.2 (30–60), MFI20 was 76.5 ± 10.6 (60–95) and sleep quality NRS was 6.9 ± 1.2 (5–9). The values of the studied parameters and scores were significantly different from the control 1.4 ± 0.5; 14.4 ± 6.5; 93.9 ± 3.5 10 ± 5.2 and 0.9 ± 0.8 respectively; p = 0.001 for all). There was a significant correlation between serum IL-6 levels and VAS-pain (r = 0.72, p = 0.001), FIQ (r = 0.58, p = 0.001), SF-36 (r = 0.78, p = 0.001), MFI-20 (r = 0.74, p = 0.001) and sleep NRS (r = 0.78,p = 0.001). On regression, IL-6 level had a greater impact on sleep NRS (p = 0.001), SF-36 (p = 0.005) and MFI20 (p = 0.01). Conclusions Serum IL-6 level is high in primary FMS patients. Also, serum IL-6 is significantly related to the parameters of fatigue, functional status, sleep quality and pain.

Immune thrombocytopenic purpura (ITP) is an acquired autoimmune hematologic disorder with heterogeneous bleeding manifestations. Many biomarkers such as interleukin-37 (IL-37), vascular endothelial growth factor A (VEGFA), and transforming growth factor-β1 (TGFß1) have a role in immunity, inflammation, and megakaryopoiesis.In the present study, immunoassay of interleukin-37 as well as the gene expression of vascular endothelial growth factor A and transforming growth factor-β1 were done in 60 primary ITP patients, 60 thrombocytopenia patients, and 60 healthy volunteers.Increased IL-37 level and down regulation of VEGFA and TGFß1gene expression were detected in primary ITP patients when compared with other groups. A negative correlation was observed between IL-37 and platelet count. However, a positive correlation was observed between VEGFA and TGFß1 levels and platelet count.Current results suggested that interleukin-37, vascular endothelial growth factor A, and transforming growth factor-β may be promising indicators in the diagnosis of ITP and detection of disease severity with inexpensive and cost-effectiveness compared to the benefits.

A high-fat, high-fructose diet (HFFD) impairs cognitive functions and increases susceptibility to neurodegenerative disorders. Irisin and heat shock protein 70 (HSP70) are well known for their role in neuroprotection. The possible neuroprotective effects of fenofibrate on HFFD-induced cognitive dysfunction and the involvement of irisin and HSP70 in these effects were investigated in this study. Rats were divided into normal control, HFFD, dimethylsulfoxide+HFFD, and fenofibrate+HFFD groups. At the end of the experiment, fenofibrate treatment restored hippocampus histological characteristics to almost normal and improved HFFD-induced cognitive deficit. It reduced body weight gain and had hypolipidemic effects by significantly lowering total cholesterol, triglycerides, and low-density lipoprotein cholesterol levels while increasing high-density lipoprotein cholesterol levels. It has antioxidant and anti-inflammatory effects as it significantly reduced the hippocampal malondialdehyde, interleukin-6, and tumor necrosis factor-alpha levels, while significantly increasing the reduced glutathione level. It prevented HFFD-induced hypoxia by significantly lowering hippocampal vascular endothelial growth factor and hypoxia-inducible factor-1 alpha levels. It significantly activated the hippocampal peroxisome proliferator-activated receptor-gamma coactivator-1 alpha (PGC-1α)/irisin/brain-derived neurotrophic factor pathway. It significantly increased hippocampal HSP70 while decreasing the HSP90 levels. It enhanced synaptic plasticity by significantly upregulating the hippocampal relative

Diabetic retinopathy (DR) is the most common diabetic neurovascular complication, and the leading cause of preventable blindness among working-age individuals. Recently, agmatine, the endogenous decarboxylated L-arginine, has gained attention as a pleiotropic agent that modulates the diabetes-associated decline in quality of life, and exhibited varied protective biological effects. Diabetes was induced by a single streptozotocin (STZ, 50 mg/kg, i.p.) injection. When diabetes was verified, the animals were randomly allocated into three groups (16 rat each); diabetic, agmatine-treated diabetic (1 mg/kg, daily, for 12 weeks), and control group. Blood glucose homeostasis, retinal redox status, apoptotic parameters, nitric oxide synthase (NOS), nitric oxide (NO), vascular endothelial growth factor (VEGF), glutamate, glutamine, glutamine synthase (GS) activity, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), and mitogen-activated protein kinase (MAPKs) pathways were assayed biochemically. Retinal vascular permeability was measured. Retinal morphology was evaluated by hematoxylin and eosin staining. Retinal N-methyl-D-aspartic acid receptor1 (NMDAR1) and glutamate aspartate transporter (GLAST) mRNA were quantified. Glucose transporter 1, pro-caspase3, and glial fibrillary acidic protein (GFAP) expression were quantified by immunohistochemistry. Chronic agmatine treatment abrogated STZ-induced retinal neurodegeneration features including gliosis, and neuronal apoptosis, restored retinal vascular permeability, mostly through antioxidant, anti-apoptotic capacity, abolishing glutamate excitotoxicity, modulating the activity of NMDARs, MAPKs/NFκB, and NOS/NO pathways. By restoring the molecular and functional background of retinal neurovascular homeostatic balance, agmatine would be appropriate therapeutic option acting upstream of the DR, impeding its progression.

Praziquantel can develop resistance and cannot counteract schistosomiasis pathology. β-glucanwas used as an immunomodulator for innate and acquired immunity. This study evaluated theeffects of β-glucan either alone or with PZQ on chronic Schistosoma mansoni infection. Micewere divided into five groups: uninfected control, infected untreated, PZQ treated, β-glucantreated and combined treatment groups. Treatment started at the end of 8th week P.I. Parasitological,histopathological, immunohistochemical (α-SMA) studies and biochemical assays (Myeloperoxidaseactivity, NO, TNF-α, INF-γ, IL-13 & hydroxyproline) in liver tissues were done.Combination of β-glucan and PZQ therapy resulted in significant decrease in adults count, hepaticegg loads, granuloma number and diameter as well as significant improvement of hepaticpathology and reduction of hepatic fibrosis.

Metadherin (AEG-1/MTDH/LYRIC) is a 582-amino acid transmembrane protein, encoded by a gene located at chromosome 8q22, and distributed throughout the cytoplasm, peri-nuclear region, nucleus, and nucleolus as well as the endoplasmic reticulum (ER). It contains several structural and interacting domains through which it interacts with transcription factors such as nuclear factor-κB (NF-κB), promyelocytic leukemia zinc finger (PLZF), staphylococcal nuclease domain containing 1 (SND1) and lung homing domain (LHD). It is regulated by miRNAs and mediates its oncogenic function via activation of cell proliferation, survival, migration and metastasis, as well as, angiogenesis and chemoresistance via phosphatidylinositol-3-kinase/AKT (PI3K/AKT), NF-κB, mitogen-activated protein kinase (MAPK) and Wnt signaling pathways. In this chapter, metadherin is reviewed highlighting its role in mediating growth, metastasis and chemoresistance in colorectal cancer (CRC). Metadherin, as well as its variants, and antibodies are associated with CRC progression, poorer prognosis, decreased survival and advanced clinico-pathology. The potential of AEG-1/MTDH/LYRIC as a diagnostic and prognostic marker as well as a therapeutic target in CRC is explored.

Allergic bronchial asthma is a long-lasting illness of the respiratory system characterized bychronic inflammation of the respiratory airways with abnormal Th2-type immune responses tospecific allergens. The accumulation of scientific evidence supports the beneficial effects ofsome parasitic infections in animal models of allergic diseases. Thus, the aim of this work wasto discover the influence of infection with T. spiralis on ovalbumin-induced acute allergic airwayinflammation in mice and to investigate whether this effect is correlated to the infectiondose or not. Therefore, the severity of respiratory airways inflammation, the leukocyte counts inthe blood and BALF, immunohistochemistry of FOXP3+CD4+T cells and the levels of IL-6, IL-13, and IL-10 were assessed. In this experiment, 120 male laboratory bred mice were randomlydivided into six groups: induced asthma, saline control, low dose preventive, high dose preventive,low dose therapeutic and high dose therapeutic groups. T. spiralis infection attenuated theintensity of pulmonary inflammation, decreased numbers of eosinophils in BALF and blood,reduced levels of IL-6 and IL-13 and elevated levels of IL-10 with a significant upregulation ofFOXP3+CD4+T cells expression compared to the uninfected induced asthma group. The preventivegroups showed the best results with no significant difference between effects of the low andthe high doses. In conclusion, T. spiralis infection reduced Th2 type infammation and augmentedregulatory immune response in ovalbumin-induced acute allergic airway inflammation withbetter preventive than therapeutic effects. Further investigations are needed to determine theminimal dose of infection that gives the best influence.

The incidence of obesity-related asthma has shown a remarkable increase. We aimed to explore the role of heat shock protein 72 (Hsp72) and receptor for advanced glycation end products (RAGE) axis with its downstream signaling in the pathogenesis of obesity-related asthma. We enrolled a total of 55 subjects and divided them into three groups. Groups I and II included healthy, normal weight (n = 15) and obese (n = 15) subjects, respectively. Twenty-five obese asthmatics (group III) were subdivided into group IIIa (10 patients with mild to moderate asthma) and group IIIb (15 patients with severe asthma). High mobility group box 1 (HMGB1), interleukin 8 (IL-8), monocyte chemoattractant protein 1 (MCP-1), extracellular signal-regulated protein kinases 1 and 2 (ERK1/2), and urinary Hsp72 were immunoassayed. Hydrogen peroxide (H2O2) and free fatty acids (FFAs) levels were photometrically measured. RAGE mRNA expression was relatively quantified by real-time PCR. We found significant elevations of serum HMGB1, IL-8, MCP1, ERK1/2, FFAs, and H2O2 levels as well as urinary Hsp72 levels in obese subjects compared to healthy control. These were more evident in patients with severe asthma (group IIIb). Multivariate regression analysis identified Hsp72 and ERK1/2 as independent predictors of bronchial asthma severity. Receiver operating characteristic (ROC) curve analysis revealed that areas under the curve (AUC) for Hsp72 and ERK1/2 were 0.991 and 0.981, respectively, which denotes a strong predictive value for identifying the severity of bronchial asthma in obese patients. The current study highlights the role of Hsp72 and HMGB1/RAGE/ERK1/2 signaling cascade in the pathogenesis of bronchial asthma and its link to obesity, which could be reflected on monitoring, severity grading, and management of this disease.

Nephropathy is a common health issue associated with type 2 diabetes mellitus (T2DM). Treatment of diabetic nephropathy (DN) in an early stage can effectively inhibit its progression. Albuminuria is the currently accepted marker for detection of DN. This study aims to evaluate the urinary level of two novel renal tubular proteins (cyclophilin A and periostin) in patients with T2DM and among different nephropathy stages and also to validate the diagnostic accuracy of both cyclophilin A and periostin as potential markers for early prediction of DN relative to albuminuria. This cross-sectional study recruited 137 patients with T2DM, and they were divided based on their urinary albumin:creatinine ratio into T2DM with normoalbuminuria ( group II), incipient T2DN with microalbuminuria ( group III) and overt T2DN with macroalbuminuria ( group IV) beside 41 healthy subjects as group I. Cyclophilin A and periostin were measured in the urine using ELISA. Diagnostic accuracy of both markers was determined for prediction of DN via receiver operating characteristic curve analyses. Urinary cyclophilin A and periostin levels were significantly higher in DN groups when compared with T2DM with normoalbuminuria group. For prediction of incipient and overt DN, areas under the curve (AUCs) of periostin were 0.954, 0.997 and cyclophilin A were 0.914, 0.937, respectively. AUCs of periostin were higher than that for cyclophilin A with a significant AUC difference (p=0.022) in overt DN stage. Periostin and cyclophilin A could be regarded as a potential urinary biomarker for early prediction of DN. Periostin exhibits a higher diagnostic accuracy than urinary cyclophilin A specifically in overt DN stage.

Early diagnosis and treatment of colorectal cancer (CRC) are important for improving patients’ survival. Metadherin is an oncogene that plays a pivotal role in carcinogenesis and can be suggested as a cancer biomarker. This study aimed to elucidate the efficacy of serum Metadherin mRNA expression as a potential non-invasive biomarker for early diagnosis of CRC in relation to other screening markers as carcinoembryonic antigen (CEA), carbohydrate antigen 19.9 (CA19.9) and Fecal occult blood (FOB) and also to assess its relationship with the tumor stage and survival rate. A convenience series of 86 CRC cases (group I) were recruited with 78 subjects as controls (group II). Serum Metadherin mRNA expression level was determined using reverse transcription polymerase chain reaction (RT-PCR). Serum Metadherin mRNA expression level was significantly elevated in CRC cases when compared with controls (P

Varicocele is a leading cause of male infertility. Melatonin is a highly pleiotropic neurohormone. We aimed to characterize the melatonin epigenetic potential in varicocele and the involved molecular mechanisms.Fifty-two male albino rats were randomly divided into four groups (13 rats each): control (I), melatonin (II), varicocele (III) and melatonin treated varicocele (IV) groups. Left varicocele was induced by partial left renal vein ligation. Reproductive hormones, epididymal sperm functional parameters, testicular 3/17 β-hydroxysteroid dehydrogenases, antioxidant enzymes, malondialdehyde, nicotinamide adenine dinucleotide phosphate oxidase, 8-hydroxy-2'-deoxyguanosine and histopathological/Johnsen's score were evaluated. Flow cytometry and Comet were carried out to explore extent of sperm and testicular DNA damage. Testicular expression of silent information regulator 1 (SIRT1), forkhead transcription factors-class O (type1) (FOXO1), tumour suppressor gene, P53, cation channels of sperm (CatSper) and steroidogenic acute regulatory protein was evaluated by western blot technique. Testicular expression of Bcl-2 and its associated X protein and nuclear factor kappa-light-chain-enhancer of activated B cells were assayed by immunohistochemical staining. Testicular miR-34a expression was quantified by quantitative reverse transcription-polymerase chain reaction.The varicocele induced testicular histological injury, enhanced oxidative stress, P53-mediated apoptosis, DNA damage and increased testicular miR-34a expression paralleled with down-regulated SIRT1/FOXO axis. Melatonin treatment of varicocele rats displayed antioxidant/anti-apoptotic efficacy and improved reproductive hormones axis, CatSper expression and fertility parameters. MiR-34a/SIRT1/FOXO1 epigenetic axis integrates testicular melatonin mediated intracellular transduction cascades in varicocele.Melatonin can be used as an adjuvant therapy to improve varicocele and its complication.

Toxoplasmosis is a deleterious parasitic disease with harmful impact on both humans and animals. The present study was carried out to evaluate the antiparasitic effect of chloroquine (CQ), spiramycin (SP), and combination of both against the highly virulent RH HXGPRT (-) strain of Toxoplasma gondii (T. gondii) and to explore the mechanisms underlying such effect.We counted the tachyzoites in the peritoneal fluid and liver smears of mice and performed scanning and transmission electron microscopy and immunofluorescence staining of tachyzoites. Moreover, relative caspase 3 gene expression was measured by real time polymerase chain reaction of liver tissues and immunoassay of anti-apoptotic markers [B cell lymphoma-2 (Bcl-2) and X-chromosome linked inhibitor of apoptosis (XIAP)] and interferon gamma (IFN-γ) was done in liver tissues by ELISA. In addition, we estimated serum levels of aspartate transaminase (AST) and alanine transaminase (ALT) and performed histopathological examination of liver sections for scoring of inflammation.We found that both CQ and CQ/SP combination significantly reduced parasitic load in the peritoneal fluid and liver smears, induced apical disruption of tachyzoites, triggered host cell apoptosis through elevation of relative caspase 3 gene expression and suppression of both Bcl-2 and XIAP. Also, they upregulated IFN-γ level, reduced serum AST and ALT, and ameliorated liver inflammation.Either of CQ and CQ/SP combination was more effective than SP alone against T. gondii with the CQ/SP combination being more efficient. Therefore, adding CQ to other anti-Toxoplasma therapeutic regimens may be considered in future research.

Aim of the work: To determine the relation between knee synovitis detected by ultrasound (US) and biomarkers of inflammation and oxidative stress in primary knee osteoarthritis (KOA) patients. Patients and methods: The study included 40 patients with primary KOA and 40 age and sex matched control. Patients were evaluated using Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) score. Laboratory investigations included high-sensitivity C-reactive protein (hsCRP), matrix metalloproteinase-mediated breakdown of CRP (CRPM), nitric oxide (NO), hydrogen peroxide (H2O2) and malondialdehyde (MDA). High resolution US examination of knee joints (grey-scale and power Doppler) was done for assessment of synovitis. Results: The patients were 37 females and 3 males, the mean age was 45.5 ± 9.25 years, 50% were housewives. Tenderness was grade 1 in 45%, 2 in 40% and 3 in 15%; 82.5% has swelling and 87.5% had crepitus; the WOMAC score was 57 (5–112); pain-index 10 ± 4.2; stiffness index 6.0 ± 2.01 and physical function 41 ± 13.55. Sonographically, 29(72.5%) had grey-scale synovitis (effusion and synovial hypertrophy) and 5(12.5%) patients had a positive Doppler signal. The serum levels of the hsCRP, CRPM, NO, H2O2 and MDA were signficantly increased in the patients compared to the control (p

Background: Previous studies showed that Heme Oxyge-nase-1 (HO-1) level was markedly reduced in Polycystic Ovary Syndrome (PCOS) which might highlight the role of HO-1system in the pathogenesis and treatment of PCOS.Aim of Study: The present study was done to study the effects of the induction of HO-1 system by hemin on Letrozole (LTZ)-induced PCOS in rats.Material and Methods: 40 female rats were divided into 4 equal groups; normal control (I), hemin (II), LTZ (III), hemin + LTZ treated (IV).Results: After three weeks, LTZ administration induced PCOS in female rats as evidenced by histological examination and biochemical analysis. It significantly increased testosterone level, LH and LH/FSH ratio compared with normal control group. LTZ significantly decreased plasma adiponectin level, ovarian Silent Information Regulator 1 level (SIRT1), Glu-tathione-S-Transeferase activity (GST), HO-1 mRNA expres-sion and ovarian B-Cell Lymphoma 2 (BCL2) expression compared with normal control group. While, it increased ovarian hydrogen peroxide (H2O2) level, ovarian BCL2 associated X (Bax) expression and Bax/Bcl2 ratio compared with normal control group. Hemin administration antagonized all these effects.Conclusion: We could conclude that, hemin is a promising drug for treatment of PCOS through its antioxidant, anti-inflammatory and anti-apoptotic effects which can rise up the possibility of involvement of HO system in pathogenesis of PCOS.

Prolonged dexamethasone (DEX) administration causes skeletal muscle atrophy through induction of both oxidative stress and mitochondrial dysfunction. Lipoxin A4 (LXA4) is a recognized antioxidant but its effect against DEX-induced muscle atrophy has not been studied yet. This study aimed to assess the potential ameliorating effect of LXA4 on DEX-induced muscle atrophy and investigate the possible involvement of the mitochondrial dynamics pathway and the redox state in this effect. Forty male rats were divided into four groups; normal control, LXA4-treated, DEX-treated, and LXA4 plus DEX-treated. At the end of the experiment, LXA4 counteracted the effect of DEX on different parameters including muscle weight, muscle strength, serum creatine kinase activity, malondialdehyde and protein carbonyl contents, Na/K-ATPase and citrate synthase activities, mitochondrial transmembrane potential, mitochondrial transcription factor (TFAM), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and nuclear factor erythroid 2-related factor 2 (Nrf2). These findings signify the promising therapeutic effect of LXA4 against DEX-induced skeletal muscle atrophy and indicate the possible involvement of LXA4-induced mitochondrial activation in addition to its well-known antioxidant effects.

Doxorubicin (DOX) is an important chemotherapeutic drug. Cardiotoxicity diminishes its clinical efficacy. We aimed to focus on the mechanism of DOX-induced cardiotoxicity, in addition, to evaluate curcumin's protective effect against it. Twenty-eight rats were divided into the normal control group I, curcumin-treated (200 mg/kg body weight [b.w.]) group II, DOX-treated (4 mg/kg b.w.) group III, and DOX + curcumin group IV. Cardiac injury markers, heart tissue oxidative stress indices, interferon-gamma (INF-γ), tumor necrosis factor-like weak inducer of apoptosis (TWEAK), upregulated modulator of apoptosis (PUMA), p53 and nuclear factor kappa-B p65 (NF-κB p65) levels as well as messenger RNA gene expression of Rac1 and fibroblast growth factor-inducible protein 14 (Fn14) were assayed, besides the assay of DNA damage, histopathological changes, survivin immunohistochemistry and electron microscopic examination. Curcumin significantly downregulated Rac1 and Fn14 gene expression and significantly decreased p53, NF-κB p65, INF-γ, and PUMA levels in the cardiac tissue. In addition, curcumin improved oxidative stress indices, DNA damage, and cardiac toxicity markers in the form of lactate dehydrogenase (LD), creatine kinase isoenzyme-MB (CK-MB), and cardiac troponin-I (cTn-I). Meanwhile, upregulated antiapoptotic marker survivin was observed. Light and electron microscopic findings confirmed our biochemical and molecular outcomes. The current study established the antioxidant, anti-inflammatory, and antiapoptotic roles of curcumin against DOX cardiotoxicity.

The current study aims to evaluate the modulatory effect of zinc oxide nanoparticles (ZnO NPs) on the bioenergetic signature biomarkers in the Ehrlich ascitic carcinoma (EAC) model. To achieve this goal, 90 female albino mice were included in this study and were divided into six equal groups (n =15 per group): saline-treated group, ZnO NP-treated, EACs-bearing mice, and three groups of EACs-bearing mice treated with ZnO NPs at a dose of 20 mg/kg every other day, 10 mg/kg every other day, 10 mg/kg every day, respectively, for 14 days. The tissues from treated groups and control groups were homogenized and used for the assay of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and F1 beta subunit of adenosine triphosphate (ATP) synthase levels, as well as the determination of lactate level. The survival time of mice was improved in all ZnO NP-treated groups, especially in EACs-bearing mice treated with ZnO NPs at a dose of 10 mg/kg every other day. This improvement was associated with an increased F1 beta subunit of ATP synthase level and a decreased GAPDH level. Also, the lactate level was significantly decreased in all treated groups when compared with the untreated group. The overall effect was the increased bioenergetic signature as compared with EC.These results implied that ZnO NPs have a significant efficacy against cancer cells and they significantly increased the bioenergetic signature.

Diabetic retinopathy (DR) is the most common diabetic neurovascular complication, and the leading cause of preventable blindness among working-age individuals. Recently, agmatine, the endogenous decarboxylated L-arginine, has gained attention as a pleiotropic agent that modulates the diabetes-associated decline in quality of life, and exhibited varied protective biological effects. Diabetes was induced by a single streptozotocin (STZ, 50 mg/kg, i.p.) injection. When diabetes was verified, the animals were randomly allocated into three groups (16 rat each); diabetic, agmatine-treated diabetic (1 mg/kg, daily, for 12 weeks), and control group. Blood glucose homeostasis, retinal redox status, apoptotic parameters, nitric oxide synthase (NOS), nitric oxide (NO), vascular endothelial growth factor (VEGF), glutamate, glutamine, glutamine synthase (GS) activity, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), and mitogen-activated protein kinase (MAPKs) pathways were assayed biochemically. Retinal vascular permeability was measured. Retinal morphology was evaluated by hematoxylin and eosin staining. Retinal N-methyl-D-aspartic acid receptor1 (NMDAR1) and glutamate aspartate transporter (GLAST) mRNA were quantified. Glucose transporter 1, pro-caspase3, and glial fibrillary acidic protein (GFAP) expression were quantified by immunohistochemistry. Chronic agmatine treatment abrogated STZ-induced retinal neurodegeneration features including gliosis, and neuronal apoptosis, restored retinal vascular permeability, mostly through antioxidant, anti-apoptotic capacity, abolishing glutamate excitotoxicity, modulating the activity of NMDARs, MAPKs/NFκB, and NOS/NO pathways. By restoring the molecular and functional background of retinal neurovascular homeostatic balance, agmatine would be appropriate therapeutic option acting upstream of the DR, impeding its progression.

Trichinellosis is a serious food-borne zoonotic infection of cosmopolitan distribution. Currently, treatment for trichinellosis is far from ideal. Given the important role of oxidative stress and immune-mediated inflammation in the pathogenesis of trichinellosis, this study was designed to evaluate the possible protective effects of resveratrol (RSV) during the intestinal and muscular phases ofTrichinella spiralisinfection in mice. The oral administration of RSV at a dose of 20 mg/kg once daily for two weeks resulted in significant reductions in both adult and larval counts; significant improvements in the redox status of the small intestine and muscles; a significant reduction in interleukin 4, pentraxin 3 and vascular endothelial growth factor expression; and the mitigation of intestinal and muscular inflammation. In conclusion, this study identifies RSV as a promising agent for the treatment of experimental trichinellosis, and more studies in experimental animals and humans are worth consideration.

Lactoferrin (LF) was previously suggested to have a protective effect against liver fibrosis by preventing hepatic stellate cells (HSCs) activation. The effect of LF on heat shock protein 47 (HSP47) has not yet been studied so this study was designed to investigate LF effect on HSP47 as a potential target for management of liver fibrosis and comparing it with silymarin (SM) in a thioacetamide (TAA)-induced liver fibrosis model. Rats were divided into four groups; normal control, TAA (TAA-treated), LF (LF + TAA-treated), and SM (SM + TAA-treated). After 6 weeks, both LF and SM improved the grade of cirrhosis, reduced collagen fibers deposition, inactivated HSCs, significantly decreased elevated liver enzymes, HSP47, hydroxyproline content, transforming growth factor-beta 1, matrix metalloproteinase-2, 8-hydroxydeoxyguanosine, malondialdehyde, nitric oxide levels and the percentage of alpha smooth muscle actin positive HSCs compared with TAA group. Moreover, LF significantly increased the total antioxidant capacity compared with TAA group. It could be concluded that LF is a promising antifibrotic drug and could be considered as one of the HSP47 inhibitors but SM is still more potent. © 2018 IUBMB Life, 70(8):795-805, 2018.

Regulatory T cells (Treg) has been documented to be protective against myocardial ischemia-reperfusion injury (MIRI). The administration of drugs which recruit Treg cells may participate in the cardioprotection of MIRI. The purpose of the present study was to investigate whether the add-on vildagliptin (vild) to standard treatment of MIRI prior to reperfusion could increase Treg recruitment, anti-inflammatory, and antioxidant effects of the standard treatment or not. Sixty diabetic patients with ST-segment elevation myocardial infarction were randomly divided into two equal groups: control group was given the standard medical treatment and vild group was given the standard medical treatment plus vild. There were no statistical differences between the mean of percentage of changes in nitric oxide, ischemia modified albumin, highly sensitive C reactive protein, and interferon-gamma levels in the studied groups. While, the percentages of changes of myeloperoxidase level, CD4+CD25+ Treg cells count, and transforming growth factor-beta1 level were significantly higher in vild group compared with control group. We concluded that addition of vild to standard medical treatment of MIRI could increase its effectiveness through recruitment of CD4+CD25+ Treg cells.

Allergic bronchial asthma is characterized by chronic inflammation of the respiratory airways mediated by T-helper 2 (Th2), Th17 and their cytokines. Although most asthmatic patients suffer from allergic airway remodeling (AAR), aggressive anti-allergic treatment failed to reverse it. The hygiene hypothesis illuminated the counter relationship between allergy and helminthic infections. The immune system is modulated by Trichinella spiralis (T. spiralis) infection to maintain homeostasis. Therefore, this work aimed to investigate the impact of chronic T. spiralis infection on induced AAR in C57BL/6 mice sensitized by house dust mites (HDM) allergens. Forty mice were divided into 3 groups: I (10 healthy mice), IΙ (15 HDM sensitized mice), and ΙΙI (15 T. spiralis chronically infected mice and sensitized with HDM allergens). The assessment aimed to evaluate the effects of regulatory CD4+CD25+FOXP3+ cells (Tregs) and their cytokines comparative to hypersensitivity mediated cytokines. Chronic T. spiralis infection effectively prevented the host's AAR. This result was evidenced by upregulated Tregs in blood by flow cytometric analysis and increased interleukin-10 (IL-10) levels in bronchoalveolar lavage (BAL) by Enzyme linked immunosorbent assay (ELISA) as well as improved lung histopathological changes. Also, serum HDM specific immunoglobulin E (IgE), BAL eosinophils, BAL IL-5 levels, and IL-17 gene expression in lung tissues were significantly reduced in T. spiralis chronically infected mice. In conclusion, the immune response in chronic T. spiralis infection could provide a promising mechanistic tool for protection against AAR, which paves the way for innovative preventive measures of other immunological disorders.

This study investigated the gastroprotective effects of N-acetylcysteine (NAC) against indomethacin-induced gastric ulcer in rats. Ulceration was induced by a single oral administration of indomethacin (30 mg/kg). 50 male albino rats were allocated into 5 equal groups: control group received normal saline orally, indomethacin group rats received normal saline orally for 5 days and indomethacin (50 mg/kg) on the last day, ranitidine group received ranitidine (reference drug) orally for 5 days (50 mg/kg) before receiving indomethacin (50 mg/kg) on the last day, and NAC groups received NAC orally at 300 and 500 mg/kg, respectively, for 5 days before receiving indomethacin (50 mg/kg) on the last day. Gastric tissue interleukin-1β (IL-1β), interferon-γ (IFN-γ), and caspase-3 levels were immunoassayed. Total thiol (T-SH), myeloperoxidase (MPO), and glucose-6-phosphate dehydrogenase (G6PD) were determined by spectrophotometry. Cytokine-induced neutrophil chemoattractant 2α (CINC-2α) gene expression was evaluated in addition to Bcl-2 immunohistochemistry. Pretreatment with NAC improved the inflammatory, apoptotic, and redox status in a dose-dependent manner particularly in NAC 500 mg/kg pretreated group. These results show a role for NAC in improving indomethacin-induced gastric ulceration via antioxidative, antiapoptotic, and anti-inflammatory interactive mechanisms.

Liver cirrhosis is a scene profitable to the advance of hepatocellular carcinoma (HCC). The current work was engrossed to weigh the potential role of Cichorium intybus linn against thioacetamide (TAA)-induced liver cirrhosis and their probable underlying biochemical and molecular mechanisms. farnesoid-X-receptor (FXR) expression, proliferating cell nuclear antigen (PCNA) immunoreactivity, and activated AMP protein kinase (pAMPK), sirtuin-1 (SIRT1), and interleukin-6 (IL6) levels were estimated in hepatic tissue by real-time PCR, immunohistochemistry, and immunoassay, respectively. C. intybus linn supplementation caused a significant improvement in serum liver enzymes, albumin, bilirubin levels, tissues redox status and hepatic histological features in addition to decreased IL6 level, hydroxylproline content, and PCNA immunoreactivity. On contrary, increased pAMPK/SIRT1 levels and upregulated FXR gene expression were observed. C. intybus linn could feasibly protect against TAA-induced hepatic damage, fibrosis, and cirrhosis by relieving oxidative stress and by interruption of the inflammatory pathway via AMPK/SIRT1/FXR signaling. PRACTICAL APPLICATIONS: No specific therapies are available until now to target the underlying mechanisms for protection against liver diseases. Herbal protection is widely available and cheap with no side effect. Cichorium intybus linn, a natural supplement, is proved in this current work to have the potential of being hepatoprotectant, antioxidant, and anti-inflammatory agents, thus reducing the risk of hepatic cirrhosis.

Conventional anthelmintics such as albendazole could not achieve complete cure of trichinellosis till now. The antimalarial mefloquine mediates oxidative stress and disrupts lysosomal functions leading to cell death. Therefore, the aim of this work was to investigate the effect of mefloquine on experimental acute and chronic trichinellosis and to clarify the possible mechanisms of such effects. Mice were divided into four groups; Group I: Uninfected untreated control (20 mice); Group II: Infected untreated control (40 mice); Group III: infected and treated with albendazole (400 mg/kg) (40 mice); Group IV: infected and treated with mefloquine (300 mg/kg) (40 mice). All infected treated groups were equally subdivided into 2 subgroups; (a) treated on the 2nd day post infection (dpi) for 3 days, (b) treated on the 35th dpi for 5 days. Parasitological adults and larvae counting besides immunohistopathological examination of intestines and muscles were done. Biochemical assay of oxidant/antioxidant status, apoptotic, cytoprotective and inflammatory biomarkers in intestinal and muscle homogenates were achieved. Results showed that both albendazole and mefloquine significantly reduced adults and larvae counts with higher efficacy of albendazole in the intestinal phase and superiority of mefloquine in the muscle phase. The superiority of mefloquine was indicated by increased inflammatory immune infiltration and decreased anti-apoptotic immunohistochemical markers expression in both jejunal and muscle tissues. Biochemically, mefloquine treatment showed highly significant oxidative, apoptotic and inflammatory effects. So, our results suggest that mefloquine might be a superior treatment for chronic trichinellosis.

Objective Inflammatory bowel diseases (IBD) are chronic and recurrent disorders of the gastrointestinal tract with unknown etiology and have two major forms, ulcerative colitis (UC) and Crohn diseases. In view of the adverse effects and incomplete efficacy of currently administered drugs, it is essential to investigate new and harmless drugs with more desirable beneficial effects. Statins have many additional pleiotropic effects other than their lipid-lowering effect. This study aims to investigate the role of simvastatin (SIM) at different doses against induced UC in rats. Methods SIM (10, 20 mg/kg), and sulfasalazine as a standard therapy (100 mg/kg) were given from five days before and seven days after induction of UC by acetic acid (AA). Colonic mucosal inflammation was evaluated macroscopically and microscopically. Furthermore, the colonic tissue tumor necrosis factor-α (TNF-α), interleukin 1beta (IL 1B), nod-like receptor family pyrin domain-1 containing 3 (NLRP3), malondialdehyde (MDA), reduced glutathione (GSH) and super oxide dismutase (SOD) were assayed in addition to immunohistochemistry of caspase-1 and cyclooxygenase-2 (COX2). Results SIM in a dose dependant manner significantly improved macroscopic and histological scores, diminished colonic levels of IL 1B, TNF-α, NLRP3, MDA, caspase-1 and COX2 and elevated GSH and SOD. Conclusion SIM has anti-inflammatory, cytoprotective and antioxidants effects that are not directly related to its cholesterol lowering activity against AA induced colitis this makes it a new therapeutic target for UC.

Corticosteroids are used to treat a variety of diseases like bronchial asthma. However, long-term corticosteroids have a gastric ulcerogenic potential. Montelukast (MTK) and Nigella sativa oil (NSO) are used in treatment of bronchial asthma. Previous studies showed that MTK and NSO had gastroprotective effects in other models of gastric ulcer. The present study assesses synergistic gastroprotective effects of both drugs in dexamethasone (DXM)-induced gastric damage. Fifty male rats were divided into 5 groups: normal control (I), DXM group (II), MTK + DXM group (III), NSO + DXM group (IV), MTK + NSO + DXM group (V). After 7 days, stomachs were removed for biochemical analysis and histological examinations. Significant increases in malondialdehyde (MDA) level, superoxide dismutase (SOD) activity, myeloperoxidase (MPO) activity, and proliferating cell nuclear antigen (PCNA) positive cells, with significant decreases in mucus secretion were detected in DXM-treated group compared with group I. Meanwhile, significant decreases of MDA level, MPO activity, and PCNA positive cells and significant increases in mucus secretion were detected in treated groups compared with group II. SOD activity significantly decreased in group V compared with group II. We could conclude that administration of either MTK or NSO or both with DXM counteracts DXM-induced gastric lesions.

Introduction: Atrazine (ATR), a worldwide triazine herbicide, induces oxidative stress and DNA damage. It was found that oxidative stress is closely linked to apoptosis. Curcumin has strong antioxidant, antimicrobial, anticancer and anti-inflammatory actions. Aim of the study: The aim of this study was to assess the possible ameliorative effect of curcumin on ATR- induced oxidative stress, oxidative DNA damage, mitochondrial dysfunction, and apoptosis in the kidney of adult male albino rats. Material and methods: The current study was conducted on 40 adult male albino rats. Rats were divided into four equal groups. The first group was control. Group II was treated with curcumin (100mg/kg/day). Group III was treated with ATR (400mg/kg/day). Group IV was treated with both ATR (400mg/kg/day) and curcumin (100mg/kg/day). All were given orally for 21days. Body and kidney weights, blood urea and creatinine as well as 24 hours urinary protein levels were measured. Levels of malondialdehyde (MDA), reduced glutathione (GSH), and 8-Hydroxy-2′-deoxyguanosine (8- OHdG) as well as activities of catalase (CAT), heme oxygenase-1 (HO-1) and complex-1 were assessed. Histopathological and immunohistochemical examination of renal tissue were carried out. Results: ATR treated group was significantly decreased in body and kidney weights, GSH level and HO-1 as well as complex 1 activities while there was significant increase in blood urea, creatinine, 24 hours urinary protein, MDA and 8-OHdG levels as well as CAT activity. Renal cloudy swelling was observed in H&E sections. Caspase 3 immunohistochemistry revealed high rate of apoptosis. Curcumin administration along with ATR significantly improved these observations. Conclusion: It was concluded that administration of curcumin along with ATR ameliorated oxidative stress, DNA damage, mitochondrial dysfunction and apoptosis induced by ATR. Recommendations: The current study recommend further studies to clarify issues related to human exposure to ATR and the ameliorative effect of curcumin in Egypt and elsewhere around the world.

Atrazin is currently the most widely used herbicide in agriculture with lots of adverse effects on human health. Curcumin is a polyphenol known for its antioxidant, anti-inflammatory, and anticancer properties. In the present study, the protective effect of curcumin on atrazin-intoxicated rats is evaluated. Toxicity was induced by oral administration of atrazine (400 mg/kg/day) for 3 weeks. Curcumin at a dose of 400 mg/kg/day was given simultaneously by oral route. Redox status, mitochondrial function, 8-hydroxydeoxyguanosine (8-OHdG) level by immunoassay, and caspace-3 expression by immunohistochemistry were evaluated. Curcumin showed significant cardiac protection with improvement of redox status, mitochondrial function, 8-OHdG level, caspase-3 immunoreactivity, and cardiac muscle degeneration. From this current study, it can be concluded that administration of curcumin improved atrazine-induced cardiotoxicity through its modulatory effect on redox status, mitochondrial function, and caspase-3 expression.

Background: Schistosomiasis is a parasitic disease causing chronic ill health in humans with a serious consequences for socio-economic development in tropical and subtropical regions. There is also evidence linking Schistosoma mansoni to colonic carcinoma occurrence. The aim of this study was to evaluate some inflammatory and oxidative stress biomarkers, as well as L-fucose as linkers between intestinal schistosomiasis and colonic dysplasia development in mice. Materials and Methods: This study was conducted upon 80 mice that were divided the control group (10 non infected mice) and infected group which was subdivided into 7 sub-groups (10 mice each) according to the time of sacrifaction in the post infection (p.i.) period, 10 mice being sacrificed every two weeks from 6 weeks p.i. to 18 weeks p.i. Tumor necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), and pentraxin 3 (PTX3) levels were estimated by immunoassay. The L-fucose level, and thioredoxin reductase (TrxR) and lactate dehydrogenase (LDH) activities were also evaluated in colonic tissue. Results: The current study revealed statistically significant elevation in the studied biochemical markers especially at 16 and 18 weeks p.i. The results were confirmed by histopathological examination that revealed atypical architectural and cytological changes in the form of epithelial surface serration and nuclear hyper-chromatizia at 14, 16 and 18 weeks p.i. Conclusions: inflammation, oxidative stress and L-fucose together may form an important link between Schistosomal mansoni infection and colonic dysplasia and they can be new tools for prediction of colonic dysplasia development in experimental schistosomiasis.

Background: Overweight and obesity are recognized as major drivers of cancers including breast cancer. Several cytokines, including interleukin-6 (IL-6), IL-10 and lipocalin 2 (LCN2), as well as dysregulated cell cycle proteins are implicated in breast carcinogenesis. The nuclear, casein kinase and cyclin-dependent kinase substrate-1 (NUCKS-1), is a nuclear DNA-binding protein that has been implicated in several human cancers, including breast cancer. Objectives: The present study was conducted to evaluate NUCKS-1 mRNA expression in breast tissue from obese patients with and without breast cancer and lean controls. NUCKS-1 expression was correlated to cytokine profiles as prognostic and monitoring tools for breast cancer, providing a molecular basis for a causal link between obesity and risk. Materials and Methods: This study included 39 females with breast cancer (G III) that was furtherly subdivided into two subgroups according to cancer grading (G IIIa and G IIIb) and 10 control obese females (G II) in addition to 10 age-matched healthy lean controls (G I). NUCKS-1 expression was studied in breast tissue biopsies by means of real-time PCR (RT-PCR). Serum cytokine profiles were determined by immunoassay. Lipid profiles and glycemic status as well as anthropometric measures were also recorded for all participants. Results: IL-6, IL-12 and LCN2 were significantly higher in control obese and breast cancer group than their relevant lean controls (p

Trichinellosis is a zoonosis acquired by the ingestion of undercooked meat containing the infective larvae of Trichinella spiralis (T. spiralis). Despite veterinary public health efforts to control it, re-emergence of the disease has been observed in many areas of the world in the past 10–20 years. Although ivermectin (IVM) achieved high efficacy as larvicidal in trichinellosis, the possibility of disease transmission to other hosts is still present that will hinder the eradication of that serious disease. Therefore, our goal is to determine the efficacy of IVM on the subsequent infectivity of T. spiralis larvae in experimental animals through parasitological and biochemical studies of the intestinal phase. We found that the proinflammatory cytokine; interleukin-1β (IL-1β) and epithelial neutrophil activating peptide 78 (ENA-78) mRNA expression were decreased in group II which was infected by IVM- treated T. spiralis larvae on the 5th day post infection, also the same group showed the lowest levels of vasoactive intestinal peptide (VIP) and protein carbonyl (PCO) as well as the lowest activities of myeloperoxidase (MPO) and superoxide dismutase (SOD) enzymes. The lowest adult and larval counts were observed in group II at the 5 th day post infection with highly significant differences in comparison to other groups. In conclusion, IVM appears to affect the infectivity of T. spiralis larvae with subsequent decrease of T. spiralis adults and total larval count. These effects were more pronounced when IVM was given early in the infection. IVM is feasible and useful drug in the treatment of current infection and control of subsequent infections with T. spiralis.

Organophosphorus poisoning is a major global health problem with hundreds of thousands of deaths each year. Research interest in N-acetylcysteine has grown among increasing evidence of the role of oxidative stress in organophosphorus poisoning. We aimed to assess the safety and efficacy of N-acetylcysteine as an adjuvant treatment in patients with acute organophosphorus poisoning. This was a randomized, controlled, parallel-group trial on 30 patients suffering from acute organophosphorus poisoning, who were admitted to the Poison Control Center of Tanta University Emergency Hospital, Tanta, Egypt, between April and September 2014. Interventions included oral N-acetylcysteine (600 mg three times daily for 3 days) as an added treatment to the conventional measures versus only the conventional treatment. Outcome measures included mortality, total dose of atropine administered, duration of hospitalization and the need for ICU admission and/or mechanical ventilation. A total of 46 patients were screened and 30 were randomized. No significant difference was found between both groups regarding demographic characteristics and the nature or severity of baseline clinical manifestations. No major adverse effects to N-acetylcysteine therapy were reported. Malondialdehyde significantly decreased and reduced glutathione significantly increased only in the NAC-treated patients. The patients on NAC therapy required less atropine doses than those who received only the conventional treatment; however, the length of hospital stay showed no significant difference between both groups. The study concluded that the use of N-acetylcysteine as an added treatment was apparently safe, and it reduced atropine requirements in patients with acute organophosphorus pesticide poisoning.

Bronchopulmonary dysplasia (BPD) is a respiratory distress syndrome caused by chronic lung parenchymal injury, occurring primarily in preterm infants. Therefore, research for early biomarkers for BPD is really important. This study was conducted to evaluate levels of Krebs Von den Lungen-6 (KL-6) and adiponectin in cord blood, neutrophil-gelatinase-associated lipocalin 2 (NGAL2) mRNA gene expression in broncho-alveolar lavage and urinary beta 2 microglobulin (β2MG) for early prediction of lung injury or possible involvement of those molecules in BPD pathogenesis and development. Method: this study was carried out from September 2012 to December 2013 with 58 preterm neonates of gestational age ≤32 weeks. KL-6, adiponectin and urinary β2MG levels by immunoassay, NGAL2 mRNA level by real-time PCR were determined. Results: cord blood KL-6, urinary β2MG and broncho-alveolar lavage (BAL) fluid NGAL2 mRNA expression levels were significantly increased, while a non-significant decrease in cord blood adiponectin level in BPD preterm relative to preterm without BPD were observed, with the best sensitivity and specificity were for KL-6 and β2MG relative to preterm without BPD. Conclusion: NGAL2, KL-6, and urinary β2MG may have role in early prediction and development of BPD in preterm neonates that may help in early prevention and treatment for better prognosis and outcome.