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BackgroundAcute renal failure (ARF) is a common clinical problem with grave prognosis and limited therapeutic modalities. Current therapeutic options for ARF are limited to supportive procedures and preventive care, none of which have been definitively shown to alter mortality.ObjectiveThe purpose o

Introduction: The non-steroidal anti-inflammatory drug (NSAID) Piroxicam is widely used especially in treatment of osteoarthritis and rheumatoid arthritis. However, it has many side effects; the most common of them is gastrointesti nal intolerance and ulceration. The Nigella Sativa Oil (NSO) was reported to have anti-inflammatory and antioxidant properties. Aim of the Work: To investigate the histopathological effects of piroxicam on the gastric mucosa of adult male albino rats and the possible protective role of Nigella Sativa Oil (NSO). Materials and Methods: Fourty adult male albino rats were randomized into 4 groups (NN10). They received 2 ml of the following oral treatments through an orogastric tube: Group I (Control) received a single dose of saline, Group II (NSO) received a single dose of NSO; 10 ml/kg BW, Group III (Piroxicam) received piroxicam 20 mg/kg BW and Group IV (NSO/ piroxicam) received NSO one hour before administration of piroxicam. The gastric mucosa from the body of the stomach was processed for histological stains (H&E and PAS) and for examination with scanning electron microscope (SEM). Results: Piroxicam produced erosions, congestion, extravasated RBCs and inflammatory cell infiltration. It also led to increase in the gastric mucus. The SEM results revealed marked damage of the gastric mucosal surface and complete loss of the normal architecture. In NSO prior to piroxicam group, the structure of the mucosa was nearly similar to control by both light and SEM however, there was marked increase in mucus secretion. Conclusion: NSO can partly protect the gastric mucosa against piroxicam induced damage.

Background: Acute pancreatitis (AP) is a disease that still has high morbidity and mortality rates. Oxygen free radicals and cytokines have been mentioned to play a role in the development of L-arginine induced AP. There is no specific therapy for AP. Herbals, as botanical medical treatments, have generated a deal of public controversy in recent years. Wheat germ oil (WGO) is one of these treatments that possess anti-inflammatory properties. Objective: To investigate the possible protective and therapeutic effect of wheat germ oil on L-arginine induced AP in adult albino rats. Methods: Forty adult male albino rats were divided equally into five groups: Group I (control group). Group II (WGO group): received WGO by oral gavage once daily for 3 successive days. Group III (AP group): received double IP injection of L-arginine with 1 h interval. Group IV (protection group): received WGO as group II, followed by Larginine injection as group III. Group V (therapeutic group): received L-arginine followed by WGO. Blood samples were taken for biochemical assessment of serum lipase to confirm induction of AP. At the end of the experiment, animals were sacrificed and specimens from head of the pancreas were taken and prepared for light, electron microscopic examinations and ELISA detection of interleukin-1β. Results: AP and protected groups showed extensive acinar cell damage in the form of loss of basal basophilia, necrotic changes, interstitial edema, severe inflammatory infiltration and hemorrhage. These groups showed statistical significant increase in the mean of pancreatic damage compared to control group (p

Background: DEHP is a commonly used phthalate plasticizer in polyvinylchloride (PVC) formulations used by many medical devices. It is known to be released with time into the biological fluids or redistributed into various tissues increasing the risk of certain health hazards that include developmental anomalies, reproductive and respiratory health effects. Objective: To investigate the histopathological effects of DEHP on the lung alveolar tissues and the possibility of recovery after stoppage of DEHP administration in adult albino rats. Methods: Thirty adult male albino rats were divided equally into three groups, received the following via orogastric intubation once daily for 2 weeks: Group I (control group): received normal saline. Group II (DEHP treated group): received DEHP dissolved in normal saline. Group III (DEHP recovery group): received DEHP as group II and then left untreated for another 2 weeks. The right lung from each animal was dissected, cut into small pieces. Some specimens were processed for paraffin sections to be stained with Haematoxylin & Eosin and Masson’s trichrome, others were processed for semi-thin sections, and ultrathin sections to be examined with Transmission Electron Microscope. Results: The alveolar tissue in DEHP treated group showed marked increase in the thickness of the interalveolar septa with collagen deposition and inflammatory cellular infiltration associated with many collapsed alveoli. Most of type II pneumocytes showing necrotic changes in the form of vacuolated or deeply acidophilic cytoplasm with karyorrhetic or pyknotic nuclei. Additionally, there was interstitial hemorrhage. We found a statistically significant increase in the thickness of the interalveolar septa, number of type II pneumocyte, number of alveolar macrophages/field and the area percentage of collagen fibers when compared to control group. Ultrastructurally, type II pneumocytes showed degenerative changes in the form of cytoplasmic vacuolation and destruction of lamellar bodies and mitochondria. However, alveolar tissue changes showed mild improvement after drug stoppage. Conclusion: DEHP has toxic effect on the alveolar tissues which was not totally improved after its withdrawal.