Histological and Physiological Studies of the Effect of Bone Marrow-Derived Mesenchymal Stem Cells on Bleomycin Induced Lung Fibrosis in Adult Albino Rats

BACKGROUND@#Lung fibrosis is considered as an end stage for many lung diseases including lung inflammatory disease, autoimmune diseases and malignancy. There are limited therapeutic options with bad prognostic outcome. The aim of this study was to explore the effect of mesenchymal stem cells (MSCs) derived from bone marrow on Bleomycin (BLM) induced lung fibrosis in albino rats. @*METHODS@#30 adult female albino rats were distributed randomly into 4 groups; negative control group, Bleomycin induced lung fibrosis group, lung fibrosis treated with bone marrow-MSCs (BM-MSCs) and lung fibrosis treated with cell free media. Lung fibrosis was induced with a single dose of intratracheal instillation of BLM. BM-MSCs or cell free media were injected intravenously 28 days after induction and rats were sacrificed after another 28 days for assessment. Minute respiratory volume (MRV), forced vital capacity (FVC) and forced expiratory volume 1 (FEV1) were recorded using spirometer (Power lab data acquisition system). Histological assessment was performed by light microscopic examination of H&E, and Masson’s trichrome stained sections and was further supported by morphometric studies. In addition, electron microscopic examination to assess ultra-structural changes was done. Confocal Laser microscopy and PCR were used as tools to ensure MSCs homing in the lung. @*RESULTS@#Induction of lung fibrosis was confirmed by histological examination, which revealed disorganized lung architecture, thickened inter-alveolar septa due excessive collagen deposition together with inflammatory cellular infiltration. Moreover, pneumocytes depicted variable degenerative changes. Reduction in MRV, FVC and FEV1 were recorded. BM-MSCs treatment showed marked structural improvement with minimal cellular infiltration and collagen deposition and hence restored lung architecture, together with lung functions. @*CONCLUSION@#MSCs are promising potential therapy for lung fibrosis that could restore the normal structure and function of BLM induced lung fibrosis.

Histological and Physiological Studies of the Effect of Bone Marrow-Derived Mesenchymal Stem Cells on Bleomycin Induced Lung Fibrosis in Adult Albino Rats

BACKGROUND@#Lung fibrosis is considered as an end stage for many lung diseases including lung inflammatory disease, autoimmune diseases and malignancy. There are limited therapeutic options with bad prognostic outcome. The aim of this study was to explore the effect of mesenchymal stem cells (MSCs) derived from bone marrow on Bleomycin (BLM) induced lung fibrosis in albino rats. @*METHODS@#30 adult female albino rats were distributed randomly into 4 groups; negative control group, Bleomycin induced lung fibrosis group, lung fibrosis treated with bone marrow-MSCs (BM-MSCs) and lung fibrosis treated with cell free media. Lung fibrosis was induced with a single dose of intratracheal instillation of BLM. BM-MSCs or cell free media were injected intravenously 28 days after induction and rats were sacrificed after another 28 days for assessment. Minute respiratory volume (MRV), forced vital capacity (FVC) and forced expiratory volume 1 (FEV1) were recorded using spirometer (Power lab data acquisition system). Histological assessment was performed by light microscopic examination of H&E, and Masson’s trichrome stained sections and was further supported by morphometric studies. In addition, electron microscopic examination to assess ultra-structural changes was done. Confocal Laser microscopy and PCR were used as tools to ensure MSCs homing in the lung. @*RESULTS@#Induction of lung fibrosis was confirmed by histological examination, which revealed disorganized lung architecture, thickened inter-alveolar septa due excessive collagen deposition together with inflammatory cellular infiltration. Moreover, pneumocytes depicted variable degenerative changes. Reduction in MRV, FVC and FEV1 were recorded. BM-MSCs treatment showed marked structural improvement with minimal cellular infiltration and collagen deposition and hence restored lung architecture, together with lung functions. @*CONCLUSION@#MSCs are promising potential therapy for lung fibrosis that could restore the normal structure and function of BLM induced lung fibrosis.

Detection of Helicobacter antigen in stool samples and its relation to H. Pylori positive cholecystitis in Egyptian patients with chronic calcular cholecystitis

Evidences supporting the association between H. pylori infection and chronic cholecystitis could be found by using direct culture or staining of H. pylori in gallbladder tissues as well as indirect techniques. Stool antigen test has been widely used due to its non-invasive nature. Various stool antigen tests were developed to detect H. pylori using an enzyme immunoassay [EIA] based on monoclonal or polyclonal antibodies This study evaluated the frequency of H. pylori antigen in stool samples of patients with chronic calcular cholecystitis as regard gall bladder histopathological changes. -Fifty patients were included presented with symptomatic cholecystolithiasis recruited from the outpatient clinic of National Hepatology and Tropical Medicine Research Institute during 2014-2015. Full history and clinical examination and abdominal ultrasonography were performed. Stool samples were collected, prepared and examined for detection of H. pylori antigen. Cholecystectomy was done for all patients; 45 patients [90%] by laparoscopic Cholecystectomy and 5 patients [10%] by open surgery and removed gallbladders were submitted to pathology department for detection of H. pylori in tissue under microscope using Giemsa stain. The results showed that [82%] were females with mean age [42.6+1years]. The mean BMI was [29+7.2] H. pylori-specific antigen in stool samples was detected in 40% of patients and38% were detected in patients; tissue, with significant correlation between H. pylori-specific antigen in stool and in tissue. Histopathological pictures infection in tissue were 68.4% mucosal erosions, 63.2% mucosal atrophy, 57.9% mucosal hyperplasia, 26.3% metaplasia, 42.1% musculosa hypertrophy, 26.3% fibrosis, but lymphoid aggregates were in 42.1% of cases

Immunohistochemical study on the effect of soft diet and omega 3-fortified soft diet on neurogenesis in the rat dentate gyrus and the subventricular zone

Adult brain neurogenesis persists in the subventricular zone [SVZ] and in the subgranular zone [SGZ] of the dentate gyrus. Modulation of neurogenesis by diet is a mechanism by which nutrition affects memory, learning, and mood. To study the effect of the soft diet with or without omega 3 fatty acids on neurogenesis. Thirty weaned male albino rats [3 weeks] were divided into three groups. Group 1 [control group] were fed on hard diets, group 2 were fed on soft diets, and group 3 were fed on soft diets plus omega 3 fatty acids for 3 months. Nerve cell proliferation in the SVZ and the SGZ was detected immunohistochemically using thymidine analog bromodeoxyuridine [BrdU]. The results were statistically analyzed. In the dentate gyrus, there was a significant increase in the number of BrdU-positive cells in groups 1 and 3 compared with group 2. Meanwhile in the SVZ, there was a significant increase in the number of BrdU-positive cells in group 3 compared with group 1. In group 1, the newly formed cells in the SGZ reached the granular cell layer of the dentate gyrus. The newly formed cells in the SVZ reached the olfactory bulb [OB] after 2 weeks but failed to survive for 4 weeks in the OB. In group 2, few newly formed cells reached the granular cell layer of the dentate gyrus, but they failed to reach the OB. In group 3, the newly formed cells reached their destination in the granular cell layer of the dentate gyrus and the OB. In the OB, the cells succeeded to survive for 4 weeks and were incorporated among the granular cells of OB. Hard diet and omega 3-fortified soft diet had a stimulatory effect on the process of neurogenesis in the dentate gyrus. Meanwhile in the SVZ, fortified soft diet had more stimulatory effect on proliferation and improvement of the survival rate of the newly formed cells than the hard diet

Toxic effects of diazinon on the reproductive system of male rats: the possible ameliorative role of vitamin C

Diazinon, an organophosphorous insecticide has been used in agriculture and domestic purposes for several years. The aim of this study was to analyze the reproductive toxicity induced by diazinon which caused biochemical and ultrastructural changes in adult male Wistar rats and to evaluate the possible protective effect of vitamin C. Vitamin C [200mg/Kg, once daily], diethyl-ether [0.02 ml/Kg, once daily], diazinon [10mg/Kg, once daily in] and vitamin C [200mglKg, once daily] + diazinon [10mglKg per day, once daily] combination were given to rats orally via gavage for 4 weeks. Testicular functions were assessed by testicular sperm count, sperm motility, biochemical studies and histopathology. By the end of the 4[th] week, rats given diazinon alone had significantly lower sperm count and sperm motility than the untreated control rats. Also, the rats given diazinon had significantly lower testosterone level, higher MDA [malondialdehyde] and lower catalase levels than the control group. Co- treatment of diazinon- exposed rats with vitamin C had an ameliorative effect on sperm count, sperm motility, testosterone, MDA and catalase levels. Light microscopic investigations revealed that 4 weeks of diazinon exposure was associated with marked testicular degenerative changes. Damage of spermatogenic cells and sertoli cells were observed by electron microscope. Mild degenerative changes were observed in the semineferous tubules andinterstitial tissues in the rats which received diazinon+ vitamin C. Thus, it appears that vitamin C ameliorates diazinon testicular toxicity but is not completely protective

Upregulation of the inducible nitric oxide synthase in rat hippocampus in a model of Alzheimer's disease: a possible mechanism of aluminium induced Alzheimer's

Alzheimer's disease attacks the brain causing gradual memory loss. Alzheimer's brain showed excess beta amyloid protein and neurofibrillary tangles, containing deposition of aluminium. Increasing evidence suggests that many neurons may die through apoptosis in Alzheimer's. Inducible nitric oxide synthase [iNOS] derived nitric oxide [NO] has been implicated in this process of neuronal cell death and apoptosis. Aluminium is considered a potential etiological factor in Alzheimer's disease and was used to produce an animal model of Alzheimer's. However, the exact mechanisms of aluminium induced Alzheimer's and neurotoxicity remain largely unknown. The present study was carried out to investigate the profile of the expression of iNOS in the hippocampus in an animal model of Alzheimer's produced by aluminium administration. Twenty four adult male albino rats were divided equally into four groups. Group I was the untreated control, groups II, III and IV were given aluminium chloride [300 mg/kg body weight] orally daily for one week, two and four weeks, respectively. At the end of the experiment, rats were killed by decapitation under brief anaesthesia. The brains were removed and processed for immunohistochemistry using antibody raised against iNOS. Results: By comparison to the untreated control, aluminium treated rats showed significant [P<0.05] increase in the expression of iNOS in the hippocampus. The expression was mainly neuronal and was seen in all areas. Additionally. administration of aluminium for four weeks caused marked histological changes with significant [P <0.05] reduction in hippocampus neuronal number and distortion of neuronal morphology. These data provide further evidence that exposure to aluminium may contribute to pathogenesis of Alzheimer 's and neurotoxicity by induction ofiNOS with subsequent increase in NO production that potentiate neuronal cell death in hippocampus