Background: Adults with hypertension often suffer from peptic ulcer disease and are more likely to receive drugs for hypertension and peptic ulcer Aim of the study: The aim of this study was to evaluate effect of L-arginine and carvedilol as nitric oxide donors on peptic ulcer and on peptic ulcer hypertension co-morbidity regarding to these parameters: blood pressure, ulcer score, ulcer index, total antioxidant capacity(TAC),nitric oxide (NO), prostaglandinE2(PGE2)and tumor necrosis factor alpha (TNF-α) Methods: Rats were classified into: Group 1: control normal group.

Background: Diabetes is associated with both micro-and macrovascular complications. Aim of the study: The aim of the present study is to evaluate the prophylactic effect of HCQ alone and in combination with glimepiride and metformin on ISO induced MI in type 2 diabetic rats. The present study included the parameters blood glucose, plasma insulin, HOMA-IR index, lipid profile, AKT, ECG changes and histopathology of the myocardium. Methods:Rats were classified into: Group I: control normal group. Group II:was not treated diabetic (diseased group). Group III: was treated with HCQ. Group IV: was treated with glimepiride. Group V: was treated with metformin. Group VI: was treated with HCQ + glimepiride. Group VII: was treated with HCQ + metformin. treated groups received drugs for 4 weeks. Results: Treated groups showed significant improvement in all parameters and improvement of the histopathology of the myocardium. A significant improvement in the parameters was seen in the treated groups at the end of the 4 th week. Conclusion: Our study revealed that HCQ with glimepiride or with metformin produced more improvement in blood glucose level, insulin, HOMA-IR, lipid profile, AKT, ECG changes, histopathology of the myocardium. So, our drugs, mainly combined drugs may have a prophylactic effect against MI in diabetic rats. this may be due to their glycemic control and improvement of dyslipidemia.

Fluoxetine is a selective serotonin reuptake inhibitor (SSRI), it is used in the treatment of depression; it has a toxic effect on the testis. Major depressive disorder is a pathological disorder associated with increased levels of the inflammatory cytokines tumor necrosis factor-alpha (TNFα), interleukin-6 (IL-6), and IL-1 beta (IL-1β). Fluoxetine increase in malondialdehyde (MDA) and decrease in antioxidant enzyme activity SOD superoxide dismutase and catalase (SOD and CAT) and reduced glutathione (GSH). The study aimed to investigate whether vitamin D can reduce the oxidative damage caused by fluoxetine. Thirty -two adult male rats are divided into four groups and are included in the analysis. Animals in Group I (control group) were administered distilled water by gavage. Groups II: animals were given a dose of 10 mg/kg of fluoxetine (fluoxetine treated group) orally by gavage daily for 4 weeks. Group III (vitamin D group) animals received intramuscular VD (1,000 IU/kg; 3 days/week for 4 weeks. Group IV (fluoxetine+ vitamin D): drugs were given in the same previous doses for 4weeks. Blood samples were obtained 24 hours after the last dose of each drug. The biochemical results showed that fluoxetine significantly increased oxidative stress in testicular tissue and inflammatory markers in serum. The in-depth investigations supported that administering the fluoxetine combined with vitamin D reduced the testicular damage to a marked level and normalized all relevant markers. It was concluded that the oxidative stress induced by fluoxetine administration in rats could be reduced by vitamin D supplementation.