Curcumin (CUR) has been used since ancient times to treat several ailments as it possesses many pharmacological activities. This study intended to explore the mechanism underlying the protective effects of CUR in remodeling oxidative stress and apoptotic signals in cyclophosphamide (CP)-induced pulmonary injury in albino rats. CUR was administered at a dose of 300 mg/kg/day for 7 days and on the seventh day a single dose of CP (200 mg/kg) was given. Histopathological and ultrastructural examinations of CP-intoxicated rats showed complete alveolar obstruction, thickened inter-alveolar septa, enlarged blood vessels, severe inflammatory edema with pyknotic nuclei, and disappearance of cytoplasmic organelles. Significant increases in caspase-3, malondialdehyde (MDA), and protein carbonyl (PCO) and significant decreases in superoxide dismutase (SOD) and glutathione peroxidase (GPx) were observed. In contrast, rats that received CUR showed clear and empty lumina with single row of pneumocytes, disappearance of edema, and no interstitial electron dense bodies in rats’ lung tissues. Additionally, CUR significantly reduced caspase-3, MDA, and PCO and increased SOD and GPx. In conclusion, these findings revealed the protective effects of CUR against CP-induced pulmonary injury in rats through suppressing oxidative damage and apoptosis.
<p class="abstract"><strong>Background:</strong> Cyclophosphamide is anticancer and immunosuppressant agent used to treat malignant and autoimmune diseases. Its long-term use causes side effects, as infertility and pulmonary toxicity. Coenzyme Q10; the only synthesized antioxidant in human body, acts as powerful antioxidant, scavenging free radicals, and inhibiting lipid peroxidation. Aim of present study was to examine effect of coenzyme Q10 on blood biochemical profiles, histopathological changes in lungs of adult rats exposed to cyclophosphamide-induced toxicity.</p><p class="abstract"><strong>Methods:</strong> 36 adult male albino rats divided into four groups; control and three experimental each having 9 rats. First experimental group received coenzyme Q10, second received cyclophosphamide while third group received coenzyme Q10 along with cyclophosphamide. Experiment lasted for 7 days. On 8th day, animals were sacrificed by decapitation. Lung tissue samples were collected for histopathological examination. SOD (superoxide dismutase) and MDA (malondialdehyde) levels were determined and used for statistical analysis. </p><p class="abstract"><strong>Results:</strong> In coenzyme Q10 treated group, H&E stained sections revealed normal respiratory alveoli. Ultrathin sections revealed normal alveolar septa, pneumocyte and blood capillaries contain erythrocytes. In cyclophosphamide treated group, H&E stained sections revealed peribronchial and interstitial fibrosis. Ultrathin sections revealed alveoli having apparent free lumen with extravasated erythrocytes. Alveolar septa revealed collagen fibrils deposits, and proliferated fibroblasts. In combined coenzyme Q10 and cyclophosphamide treated group, H&E stained sections revealed marked decrease of inter-alveolar tissue thickening. Ultrathin sections revealed destructed alveolar septa with dissociated remnants of collagen fibrils. Blood capillaries appeared wide, containing monocytes and erythrocytes.</p><p class="abstract"><strong>Conclusions:</strong> Administration of coenzyme Q10 with cyclophosphamide is advised to alleviate cyclophosphamide-induced lung toxicity.</p>
<p class="abstract"><strong>Background:</strong> Sleep deprivation is verging on a public health epidemic. It induced mild organ injuries through oxidative stress. The present study aimed at evaluating possible histopathological and immunohistochemical alterations caused by sleep deprivation on the liver, heart and kidney.</p><p class="abstract"><strong>Methods:</strong> 36 Wistar senile male albino rats were divided into two groups; control and experimental. Experimental rats were placed in a plastic cage, with grid floor placed inside it. The cage was filled with water to 1 cm below the grid surface. The stainless-steel rods of the grid were set 2 cm apart from each other. Loss of muscle tone associated with sleep caused them to touch the water and wake up. At the end of the experiment, animals were sacrificed by decapitation on days 1, 3 and 5. Liver, kidney and heart were obtained and dissected. </p><p class="abstract"><strong>Results:</strong> In SSD1 group, liver cells showed early stage of hepatic steatosis while mucolipidosis within hepatocytes was detected in SSD3 and the degree of steatosis increased in SSD5. Renal glomerular congestion was detected in SSD1. In SSD3 vascular congestion of glomerular tufts and apoptosis of the lining tubular epithelium was seen. Renal casts were formed in SSD5. In SSD1 lysis of myocardial fibrils was seen. Myocardial fibers degeneration represented by increase sarcoplasmic eosinophilia in SSD3. Sarcoplasmic vacuolation and nuclear chromatolysis increased in SSD5. Staining with GFAP and P53 showed various results among the liver, heart and kidney.</p><p class="abstract"><strong>Conclusions:</strong> Sleep deprivation might induce multiple organ injury through oxidative stress causing altered histological appearance.</p>
Background: Aspartame is considered the most widely used nocaloric artificial sweetener. It is used in a variety of food products and beverages. However, the consumption of aspartame has been controversial as several studies have reported an association between its use and many serious diseases.
In this study, the effect of oral ciprofloxacin on the structure of the thoracic aorta in rats was investigated. Twenty four male albino rats were divided into 4 groups (6 rats/group): group I (adult control), group II (adult rats treated with ciprofloxacin), group III (senile control), and group IV (senile rats treated with ciprofloxacin). Rats in groups II and IV received ciprofloxacin via oral gavage in a daily dose of 3.5 mg/kg/d for 14 days, while control rats received equivalent amount of distilled water used to dissolve the drug. After 2 weeks, all rats were sacrificed, thoracic aortae were dissected, and half of the specimens were processed for paraffin sections and examined by light microscopy. The other half of the specimens were prepared for scanning electron microscopy. Sections from rats treated with ciprofloxacin showed evident damaging effect on aortic wall particularly in (group IV). Aortic intima showed, focal desquamation of the lining epithelium. Tunica media exhibited loss of the normal concentric arrangement and degeneration of the smooth muscle cells. Immune staining for alpha smooth muscle actin showed muscle damage. Interestingly, some sections in (group IV) showed out-pouch (aneurysm like) of the aortic wall. There was dense collagen fibers deposition. Scanning electron microscopic observations of (group IV) revealed uneven intima, adherent blood cells and fibrin filaments to damaged intima, and out-pouch formation. It was concluded that oral ciprofloxacin caused deleterious structural changes in the thoracic aortic wall of rats explaining clinical observations of fluoroquinolones induced risk of aortic dissection and aneurysm.
Introduction Age related degeneration (ARD) is the leading cause of irreversible blindness among old people. Epidemiologic studies have suggested that nutritional parameters such as dietary fat and cholesterol may play a role in the pathogenesis of retinal degeneration. High intake of saturated fat and cholesterol is correlated with a higher risk for early ARD which occurs either directly or through the promotion of vascular pathology. Aim of the work was to evaluate the early histological and immunohistochemical changes of the retina, induced by hypercholesterolemia in adult male albino rat and comparing these changes with similar results in aged male albino rat and to apply a comparative lipid profile biochemical study between the different groups. Materials and methods Forty male albino Sprague Dawley rats were used in the study. They were divided into four groups, ten rats per each; Group I: control adult: aged 3-6 months and group II: control aged: aged 24 months were fed on standard diet, Group III: adult hypercholesterolemic group and group IV: aged hypercholesterolemic group were fed on hypercholesterolemic diet which consisted of the same ingredients of the standard diet except for the cellulose was reduced to (4%) with addition of cholesterol (1%) for duration of 6 weeks. At the end, retinal specimens were collected and processed for light microscopic and immunohistochemical examination. Results The aged rats showed marked disruption of the normal histological architecture of retina and affection of each individual retinal layer. Hypercholesterolemia markedly affected the adult rat retina and aggravated the aged retina. The affected retinae showed marked thinning of the retinal thickness, disorganization of the cell within the neuronal cell layer with decreased number of the cells within ganglion-cell layer. Immunohistochemistry revealed significant increase in retinal reactivity to glial fibrillary acidic protein, vascular endothelial growth factor, caspase 3 and nitric oxide synthase by aging and hyperlipidaemia. Conclusion The present work suggested that hypercholesterolemia is an important risk factor that can accelerates aging of healthy adult retina producing age related retinal degeneration.
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