Eman Mosallam Mohamed

Background: Acute pancreatitis (AP) is a sudden pancreatic inflammation that has a high mortality rate, especially when associated with systemic inflammation and multiple organ failure. According to reports, cases having acute pancreatitis developed stress ulcers or gastrointestinal mucosal lesions. Nesfatin-1 could control apoptosis and inflammatory effects. Aim This research is designed to find out the possible protective role of nesfatin-1 on fundic gland mucosal affection in cerulein-induced acute pancreatitis. Methods Forty rats were splitted into three groups: Group I (control), Group II (induced acute pancreatitis): exposed to cerulein (20 μg/kg, s.c.) five times each separated by one hour, Group III (nesfatin-1 treated): nesfatin-1 (10 µg/kg) is injected intraperitoneally 5 min before the first cerulein adminstration. Results Acute pancreatitis demonstrated high serum amylase, lipase, IL-1β, and oxidative stress marker (MDA) levels. Fundic gland histological changes secondary to pancreatic injury were confirmed by H&E, immunohistochemical ( IL-1β, CD68), morphometrical, and statistical studies. The fundic glands of Group II showed mucosal disruption and desquamation of the surface epithelial cells. Cells had pyknotic nuclei and vacuolated cytosol aligned parts of the glands, while others were aligned by cells with flattened nuclei. Inflammatory cells were also seen. Many cellular infiltrations and engorged blood vessels were seen. Group III (nesfatin-1 treated) showed results similar to control group. Many fundic mucosal cells in the upper and lower parts had vesicular nuclei and few had darkly stained nuclei. The gastric pits appeared narrow. Conclusions Nesfatin-1 reduces pancreatic oxidative stress damage and reduces inflammation to decrease AP-induced fundic gland mucosal affection.

Introduction: Bronchial asthma is a multifaceted respiratory disorder that represents a significant global public health concern, afflicting millions of individuals and resulting in considerable morbidity and mortality. Aim of Work: to unravel the intricate ultra-structural and cyto-molecular potential impacts of exosomes released by mesenchymal stem cells (MSCs) as biocompatible nanocarriers of miR-146 on experimentally induced bronchial asthma. Materials and Methods: Thirty-two male adult albino rats were splitted into three groups. Group I (control group), group II (experimentally induced asthma group): Every rat got 25 µg house dust mite (HDM) extract suspended in 35 µL of saline for five sequential days weekly for four weeks intranasally, and group III (exosome-treated groups): rats were administered HDM as group II, and after two weeks, they received 100 µg MSC-derived exosomes in 0.5 ml PBS intravenous through the tail vein, once/day for two weeks. Pulmonary tissue samples were examined for histopathological, ultrastructural, and NF-κB immune expression beside RT-PCR estimation of miR-146a, IRAK1, and NF-κB. Results: observable morphological and ultrastructural restoration of pulmonary tissue architecture in the MSCs exosomes-treated group compared to induced asthma group were recorded. Furthermore, the significant suppression of IRAK1 and NF-κB, along with the expantion of miR-146a and reduced immunohistochemical representation of NF-κB in the exosomes-treated group, indicated the potential molecular mechanisms for the observed histo-morphometric impacts. Conclusion: our study outlined the therapeutic implicit of miRNA-146 in mesenchymal stem cell exosomes via IRAK1/NF-κB pathway as a novel and effective approach for managing bronchial asthma and paving the way for further research.

Introduction: Semicarbazide (SEM) has gained concerns about its existence, excessive exposure and possible hazards to the human health. Infants and children are at more risk of exposure to SEM because their high intake of food put in glass jars as jams, fruit juices, honey, sterilized vegetables, mayonnaise, mustard, sauces and ketchupsAim of Work: to estimate the effects of semicarbazide on histological ovarian structure of adult albino rats and the chance for recovery after its withdrawal.Materials and Methods: Forty-five adult female albino rats were divided into three groups. Control, semicarbazide treated (40 mg/kg body weight / day for four weeks) and withdrawal group (given SEM for four weeks as the previous group, then SEM was withdrawn for 2 weeks). Samples were gathered and examined by light and transmission electron microscopes. Changes in body weight, Gonadotrophin releasing hormone (GnRH), Luteinizing hormone (LH), Follicle stimulating hormone (FSH) and Estradiol (E2) levels were estimated.Results: SEM enhanced significant drop in body weight, GnRH, LH, FSH and E2 hormone levels as well as histopathological alterations of ovarian tissues. Ovarian alterations appeared as degenerated follicles with exfoliated cells and hyaline material in their lumen. Granulosa cells were widly separated with ill-defined corona radiata. Various ultrastructural changes in follicular cells with irregularity and thickening in basement membranes surrounding them. Many lipid droplets in the cytoplasm of granulosa lutein cells were also demonstrated. These alterations were partially reversed on withdrawal of SEM.Conclusion: Semicarbazide induced dangerous changes in rat ovarian structure. Parts of these changes were reversed after withdrawal of this agent but others were still present which have negative impact on reproductive functions.

Background: The excessive exposure to silver nanoparticles (Ag-NPs) has raised concerns about their possible risks to the human health. The brain is a highly vulnerable organ to nano-silver harmfulness. The aim of this work was to evaluate the impacts of Ag-NPs exposure on the cerebellar cortex of rats. Methods: Rats were assigned to: Control, vehicle control and Ag-NP-exposed groups (at doses of 10 mg and 30 mg/kg/day). Samples were processed for light and electron microscopy examinations. Immunohistochemical localization of c-Jun N-terminal kinase (JNK), nuclear factor kappa beta (NF-κB) and calbindin D28k (CB) proteins was performed. Analyses of expression of DNA damage inducible transcript 4 (Ddit4), flavin containing monooxygenase 2 (FMO2) and thioredoxin-interacting protein (Txnip) genes were done. Serum levels of inflammatory cytokines were also measured. Results: Ag-NPs enhanced apoptosis as evident by upregulation of Ddit4 gene expressions and JNK protein immune expressions. Alterations of redox homeostasis were verified by enhancement of Txnip and FMO2 gene expressions, favoring the activation of inflammatory responses by increasing NF-κB protein immune expressions and serum inflammatory mediator levels. Another cytotoxic effect was the reduction of immune expressions of the calcium regulator CB. Conclusion: Ag-NPs exposure provoked biochemical, cellular and molecular changes of rat cerebellar cortex in a dose-dependent manner.

Introduction: Cadmium is a toxic heavy metal naturally present in plant food and unavoidable pollutant for many dental procedures. This metal shares in toxic peroxidation and destruction of macromolecules in different tissues, besides inhibition of DNA repair enzymes. The tongue is one of the vital organs that could be affected by chronic cadmium toxicity, especially the filiform papillae and tongue skeletal muscles due to their high metabolic activity. Aim of work: to study the possible role of Zinc oxide nanoparticles (ZnO NPs) in attenuation of the structural, ultra-structural and biochemical changes in rats' tongues induced by Cadmium chloride. Materials and Methods: sixty adult male Albino rats were divided equally -according to the utilized substance- into three groups; control, Cadmium chloride (CdCl) and (CdCl+ ZnO NPs) groups; every group received the allocated materials for 4 weeks. Samples were processed for light, electron microscopic examinations and biochemical analysis (malondialdehyde; reduced glutathione; catalase; superoxide dismutase; glutathione peroxidase). Results: Cadmium produced various apparent histopathological and biochemical alterations in tongue tissues in the form of filiform papillae with blunted ends, and thick keratin plaques. Epithelial cell layers appeared with vacuolated cytoplasm and dark nuclei. Degenerated muscle fibrils with wide spaces between them and many collagen fibers. Significant decrease of tongue reduced GSH, SOD, GPx and Cat enzymes activity and significant increase in MDA level in Cadmium chloride group as compared to control group. ZnO NPs attenuated these changes and revealed pointed tipped filiform papillae, nearly normal cells and Parallel arrangements of myofibrils. The levels of reduced GSH, SOD, GPx, Cat and MDA were insignificant compared to control group. Conclusion: Zinc oxide nanoparticles (ZnO NPs) attenuated the structural and biochemical changes in rats' tongues induced by Cadmium chloride.

Introduction: Diabetes mellitus induces atrophy in splenic lymphoid follicles, which may affect the body defense mechanisms. Mesenchymal stem cells could be a practical approach to treat diabetes-induced spleen damage. Aim of work: to demonstrate the histological changes in adult albino rat's spleen after induction of diabetes and to assess the effect of injected mesenchymal stem cells (MSCs) treated with L-carnitine on alleviating these changes. Materials and Methods: Thirty adult male albino rats were divided into 3 main groups: Group I (control), Group II (diabetic): the rats were injected once with intra-peritoneal Streptozotocin (STZ) 50mg/kg and group III (Diabetic +MSCs): the animals were injected intravenously with MSCs four weeks after diabetes confirmation. All rats were sacrificed four weeks after MSC injections (8 weeks from the beginning of the experiment) and spleen specimens were processed to be examined by light microscope. Blood specimens were collected to measure glucose and insulin levels. The mRNA expression for Nrf2, IL 10 and IL 17A was measured by Real-time Polymerase Chain Reaction (RT-PCR). Results: Degenerative changes were observed in diabetic group in the form of reduced size of white pulp with many apoptotic nuclei. Widened congested red pulp, statistical significant reduction of insulin level, white pulp volume, area percent of CD4+ and nuclear factor erythroid 2 related factor 2 (Nrf2) immunoexpression and also in qRT-PCR relative gene expression of Nrf2 and IL 10. There was significant increase in blood glucose level and qRT-PCR relative gene expression of IL 17A. All changes were reversed in MSCs treated group. Conclusion: we concluded that L-carnitine pretreatment of MSCs releases a novel way to enhance MSCs therapeutic potential efficacy in spleen of experimental diabetic rats with recommendation of trying further researches for their application in other vital organs.

Alternaria toxins are emerging mycotoxins that gained considerable interest with increasing evidence of their existence and toxicological properties. There is limited research and insufficient data about their in vivo hazardous effects. We designed this study to evaluate histopathological and genotoxic in vivo impacts of alternariol (AOH) on the parotid gland as well as to assess the competency of gallic acid (GA) in reversing these effects. Forty healthy adult male Wister rats were utilized and assigned equally on control, GA, alternariol and AOH+ gallic treated groups. Parotid gland samples from experimental groups were collected and then examined for histopathological, ultrastructural and immunohistochemical examination for 4-hydroxynonenal “4-HNE as lipid peroxidation marker” as well as Comet assay for DNA damage. Additionally, parotid tissue homogenates were tested for catalase “CAT”, superoxide dismutase “SOD” and malondialdehyde “MDA” levels. Our data proved that alternariol produced various histopathological and ultrastructural alterations of parotid acini as well as significant DNA damage, significant reduction of CAT and SOD enzymatic activity and significant boosting of 4-HNE immunohistochemical expression and MDA levels as compared to control group. On the other hand, gallic acid administration almost restored histological and ultrastructural parotid architecture, 4-HNE immune-expression and biochemical levels. Ultimately, we demonstrated alternariol-induced histopathological and genotoxic alterations on parotid gland as well as the competency of gallic acid in reversing these effects.

The evaluation of the toxicological effects of titanium dioxide nanoparticles (TiO₂NPs) is increasingly important due to their growing occupational and industrial use. Curcumin is a yellow curry spice with a long history of use in herbal medicine and has numerous protective potentials such as antioxidant, antimicrobial, anti-inflammatory, and anti-apoptotic effects. Accordingly, we tested the hypothesis that curcumin could ameliorate TiO₂NP-induced cardiotoxic and genotoxic effects in adult male albino rats. For this purpose, 48 adult male albino rats were randomized into five groups; all treatment was by oral gavage once daily for 90 days: group I (8 rats), untreated control; group II (16 rats), subdivided into vehicle control IIa (8 rats) received saline and vehicle control IIb (8 rats) received corn oil; group III (8 rats) orally gavaged with curcumin dissolved in 0.5 ml corn oil at a dose of 200 mg/kg b.w./day; group IV treated with TiO₂NPs at a dose of 1200 mg/kg b.w./day (1/10 LD₅₀) suspended in 1 ml of 0.9% saline; group V treated with curcumin + TiO₂NPs (the same previously mentioned doses). Curcumin was orally gavaged for 7 days before TiO₂NPs treatment was initiated, and then they received TiO₂NPs along with curcumin at the same doses for 90 days. TiO₂NPs administration resulted in several myocardial cytomorphic changes as structurally disorganized, degenerated, and apoptotic cardiomyocytes and the newly implemented 3-nitrotyrosine immune expression rendered strong evidence that these effects derived from the cardio myocellular oxidative burden. Furthermore, comet assay results confirmed TiO₂NP-related DNA damage. Remarkably, all these changes are partially mitigated in rats treated with both curcumin and TiO₂NPs. Our results suggest that concurrent curcumin treatment has a beneficial role in ameliorating TiO₂NP-induced cardiotoxicity and this may be mediated by its antioxidative property.