كرار كريم جعين الحيدري

Abstract Cataract is a visual deterioration and one of the second common cause of the visual impairmentin the low-income countries. Surgical intervention is a first line for the treatment of cataract andthe cost of this procedure caused a pressure on people in developing countries thereby finding a well-toleratedpharmacological treatment is of a particular interest. This study was undertaken to demonstratethe potential effectof the topical curcumin on the selenite induced cataract in rat pups.Thirty-two male rat pups aged 10 days randomly assigned into 4 groups (8 rat in each group). Group 1 (sham group): rats subjected to the same condition of experiment but without induction of cataract;group2:ratssubjected to asingle injection of Na selenite;group 3: rats exposed toa single injection of Na selenite followed by a daily curcumin cream application peri-ocular for 2 weeks; group 4 (vehicle group): rats underwent a single injection of Na selenite followed by a daily cream base application peri-ocular for 2 weeks. At the end of experiments, the lens opacity assessed by slit lampexamination. Blood samples collected from animals for assessment of GSH level in Hb of erythrocyte. The results shows that the topical curcumin significantly decrease lens opacity in compared with untreated group. Furthermore, topical curcumin resulted in a marked increase in levelsof the GSH in comparison with the untreated group. This study shows that the topical curcumin has a protective impact on the selenite induced cataract in male rat pups.

Introduction: The novel COVID-19 infection, that is firstly discovered in China as an epidemic, has become a pandemic crisis worldwide resulting in an increase in fatality cases around the world, with economic and social problems. Some reports highlighted increased numbers of hospitalized patients with COVID-19 infection who suffered from the comorbid conditions, particularly those experienced with obesity. Given the possibility of deterioration of the obese patients with COVID-19, this study set out to address the relationship between the bodyweight index and severity of the clinical presentation in patients with COVID-19 infection who treated with a guideline therapy. Methods: A cross sectional study was performed in which the data for the 41 patients with different bodyweights (infected with COVID-19) were obtained and included patients treated either at home or in hospital based on the score of severity. Results: This study shows that increased bodyweight is associated with a severe clinical deterioration. Conclusion: The difference in bodyweight could be a risk factor deteriorating the clinical presentation of patients with COVID-19. Key wards: COVID-19; obesity; bodyweight index

Abstract Background: Nephrotoxicity is a serious & common side effect of aminoglycoside and is induced by generation of reactive oxygen species. Emerging evidence reveals that curcumin possesses antioxidant activity, therefore, this research was undertaken to evaluate the potential protective effects of curcumin in amiloration of nephrotoxicity induced by gentamicin in male rats. Materials and Methods: Eighteen male Spraque-Dawley rats were included in this study. They were divided randomly into three equal groups (six rats each). Groups I (Control) received only normal saline i.p, Groups II (GN) received gentamicin (100 mg/kg/day), Group III (GN+CUR) received a combination treatment gentamicin (100 mg/kg/day, i.p) & curcumin (200 mg/kg/day p.o). The duration of treatment was eight days and at the end of the study, animals were sacrificed and the blood sample was collected for assessment of renal function, blood urea & serum creatinine. Both kidneys were removed and prepared for a histopathology examination. Results: blood urea and creatinine were significantly higher (P < .05) in gentamycin treated group (group II) as compared to the control group (group I). However, the levels of these parameters in group 3 (co-treatment of gentamicin and curcumin) were significantly lower than those in group 2 (P < .05). Further, the histological score of renal damage was higher in the gentamicin group than in the control group. Combination treatment of curcumin and gentamicin (groupIII) significantly attenuated the histopathological damage. Conclusion: Curcumin attenuated gentamicin-induced renal injury in rats’ models. Keywords: gentamicin, nephrotoxicity, curcumin, antioxidant

Abstract Diabetes mellitus has repeatedly attracted attention of researchers to design different therapeutic approaches to achieve an optimal treatment for this serious health challenge. The purpose of the study is to evaluate treatment option for controlling hyperglycemia at site of glucose absorption through designing computerized and in vivo models to test a sodium-glucose symporter based drug design. In silico protein data bank (pdb) model of SGLUT was processed and analyzed for docking with edited test glycoside. Another model included determination of the dose-response relationship in rat intestinal glucose/saline perfusion with test glycoside. Our result showed that Ginsenoside revealed a dose dependent SGLUT blocking activity in a saturation kinetics curve, which was agreed with in silico model results. Keywords: SGLUT; Gensinoside; Perfusate glucose; ICM docking

Although reperfusion of an ischemic organ is essential to prevent irreversible tissue damage, it may amplify tissue injury. Thisstudy investigates the role of endogenous testosterone in myocardial ischemia reperfusion and apoptosis in male rats. Material andmethod. Twenty four male rats were randomized into 4 equal groups: Group (1), sham group, rats underwent the same anestheticand surgical procedure as the control group except for LAD ligation; Group (2), Active control group, rats underwent LAD ligation;Group (3), castrated, rats underwent surgical castration, left 3wks for recovery, and then underwent LAD ligation; and Group (4),Goserelin acetate treated, rats received 3.6 mg of Goserelin 3 wks before surgery and then underwent LAD ligation. At the endof experiment, plasma cTn I, cardiac TNF-