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Erectile dysfunction (ED) is a common healthcare issue that is defined as the incapability to achieve and/or maintain an erection enough to permit satisfactory sexual intercourse. Additionally, it is an early indicator or alert of undiagnosed cardiovascular disease, due to common pathophysiology mediated through endothelial dysfunction as well as the common risk factors in both diseases which include smoking, high cholesterol level, hypertension (HTN) and diabetes mellitus (DM), so it deserves proper investigations and

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The precise mechanism by which diabetes impairs spermatogenesis and testicular function is not exactly known. Vascular endothelial growth factor (VEGF) and poly(ADP-ribose) polymerase-1 (PARP-1) are important for germ cell homeostasis and repair of DNA respectively. The aim of this study was to investigate the correlation between diabetes-induced testicular damage and testicular VEGF and PARP-1 expression and the possible protective role of vitamin E supplementation. A total of 45 male Wistar albino rats were randomly divided into three groups: Group I (nondiabetic rats), Group II (streptozocin-induced diabetic rats) and Group III (streptozocin-induced diabetic rats treated orally with 0.4 mg/kg vitamin E). Five weeks later, testicular tissue was used for assessment of MDA concentration by colorimetry, histopathological examination and immunostaining for PARP-1 and VEGFIn diabetic rats, testicular weight, seminiferous tubule diameter and germinal epithelial thickness were decreased, basement membrane was thickened and Johnsen score decreased. Reduced VEGF and PARP-1 immunostaining were associated with decreased Johnsen score in diabetic rats. Vitamin E administration was protective against oxidative stress-associated damage evidenced by lower MDA levels, improved testicular weight, spermatogenesis and higher immunostaining for VEGF and PARP-1. Testicular VEGF and PARP-1 might therefore be helpful biomarkers for diabetic testicular damage. Administration of vitamin E may have a protective role against diabetes-induced testicular damage.

Myocardial infarction is a major cause of cardiac dysfunction. All components of the cardiac renin–angiotensin system (RAS) are upregulated in myocardial infarction. Angiotensin-converting enzyme (ACE) and ACE2 are key enzymes involved in synthesis of components of RAS and provide a counter-regulatory mechanism within RAS. We compared the cardioprotective effect of the ACE2 activator diminazene aceturate (DIZE) versus the ACE inhibitor enalapril on post acute myocardial infarction (AMI) ventricular dysfunction in rats. Adult male rats received subcutaneous injections of either saline (control) or isoproterenol (85 mg/kg) to induce AMI. Rats with AMI confirmed biochemically and by ECG, were either left untreated (AMI) or administered DIZE (AMI + DIZE) or enalapril (AMI + enalapril) daily for 4 weeks. DIZE caused a significant activation of cardiac ACE2 compared with enalapril. DIZE caused a significantly greater enhancement of cardiac hemodynamics. DIZE also caused greater reductions in heart-type fatty acid binding protein (H-FABP), β-myosin heavy chain (β-MYH), and in heart mass to total body mass ratio. These results indicated that activation of cardiac ACE2 by DIZE enhanced the protective axis of RAS and improved myocardial function following AMI, whereas enalapril was not sufficient to restore all cardiac parameters back to normal.

Background Acute myocardial infraction (AMI) is a leading cause of morbidity. As anti-diabetic drugs affect the cardiovascular risk of diabetic patients independent of their glucose lowering effect, this study was aimed to explore the cardioprotective effects of metformin, sitagliptin and dapagliflozin on electrocardiogram (ECG) changes, IL-1β, troponin I, caspase 3 in isoprenaline (ISO) induced MI in non-diabetic rats. The present study was conducted on 40 adult male Wistar albino rats. The rats were randomly assigned into 5 groups, 8 each: I-Normal Control (NC) group, II-ISO-induced MI control (ISO-MI) injected with ISO subcutaneously at a dose of 100 mg/kg to induce experimental AMI. III-A- Metformin treated ISO-induced MI group (300 mg/kg/day), III-B-Sitagliptin treated ISO-induced MI group (10 mg/kg/day) and III-C- Dapagliflozin treated ISO-induced MI group (5 mg/kg/day). Results Treated groups showed significant improvement at p < 0.05 of ECG parameters with a decrease HR, ST amplitude and QT interval as compared to ISO-MI group. There was significant reduction at p < 0.05 of serum levels of IL-1β, troponin I and caspase 3 in the treated groups. Conclusions All medications proved to be effective in alleviating the harmful effects caused by ISO-induced MI evidenced by ECG readings and biochemical parameters. However, Dapagliflozin demonstrated a superior effect to Metformin and Sitagliptin.

Introduction: The prevalence of Glucocorticoids (GC) use made Glucocorticoid induced osteoporosis (GIO) an important form of secondary osteoporosis. Bisphosphonates (Alderonate) are considered as pharmacological agents in prevention and treatment of GIO. Garlic containing Diallyl disulfide (DAS) has received special attention for its beneficial effects as an antioxidant. The present study attempted to evaluate the Alendronate, DAS, and the combination of Alderonate and DAS effect on bone gene expression of RANKL and OPG, serum biochemical parameters [Ca, P, alkaline phosphatase (ALP)] and histological assessment of tibia in animal model of GIO. Material and Method: Fifty pathogen albino male rats were allocated in five groups:Control group(C), Methyl prednisolone group (M), methyl prednisolone Aldenronate group (A) Methyl prednisolone Diallyl disulfide (D), Diallyl disulfide Alendronate Methyl prednisolone (AD) group.Gene expression studies, biochemical parameters, histological and morphometric studies were assessed for all animals. Results: Among the study groups, Methyl prednisolone exposure provoked decrease in OPG (0.26±0.16) increase in RANKL (3.57±.39) gene expression, decrease in serum ALP(85.38±6.3),Ca(6.41±0.89), P(1.9 ±0.35) levels and decrease in trabecular thickness (57.01±23.22).Alderonate and Dially disulfide concomitant administration was shown to increase OPG(2.84 ±0.53)and decrease in RANKL (0.63 ± 0.27) gene expression, increase serum ALP(187.75±24.93),Ca(10.330 ±.69)and P(3.16 ±0.43) levels,increase trabecular thickness(154.7±31.7)(p<0.001). Conclusion: Diallyl disulfide can add advantage to Alderonate in treatment of glucocorticoid induced osteoporosis.

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