Back ground:Atherosclerosis is the major cause of death. The most common risk factors are hyperlipidemia, diabetes, and other factors like chronic infection and inflammation.Objective:This study was undertaken to assess the effect of sitagliptin on atherosclerosis via interfering with inflammatory and oxidative pathways.Materials and Methods:A total of 18 local domestic male rabbits were included in this study. The animals were randomly divided into three groups (6 rabbits in each group): Group I normal were fed with chow (oxiod) diet for 12 weeks. Group II were fed with 1% cholesterol enriched diet for 12 weeks. Group III rabbits fed with cholesterol enriched diet for 6 weeks, and then continued on cholesterol enriched diet and treated with sitagliptin 125 mg/kg/day orally for the next 6 weeks. Blood samples were collected at the start of the study, at 6 weeks of the study and then at the end of treatment to measure serum lipids profile, hsCRP and TNFα. At end of the study, the aorta was removed for measurement of MDA, glutathione and, aortic intima-media thickness.Results:Sitagliptin results in a significant reduction (p < 0.05) in serum level of total cholesterol (TC), triglycerides (TG), high sensitive C-reactive protein (hsCRP) and TNFα with a significant increase (p < 0.05) in serum HDL level. There was a significant reduction (p < 0.05) in aortic MDA, in comparison to the untreated control group. Furthermore, sitagliptin causes significant increment (p < 0.05) in aortic GSH in comparison to induced untreated group. Regarding histopathological results, sitagliptin results in a significant reduction (p < 0.05) in atherosclerotic lesions in comparison to the induced untreated group and significant reduction in aortic intima-media thickness (p < 0.05).Conclusion:Sitagliptin reduced atherosclerosis progression in hyperlipidemic rabbit via its effect on lipid parameters and interfering with inflammatory and oxidative stress.

The aim: This research was conducted to assess the possible neuroprotective effect of Tocilizumab in brain ischemic reperfusion injury in rats. Materials and methods: 24 adult Sprague-Dawley rats were divided into four groups randomly. The sham group was given anesthesia at the same time as the other groups and was in the same condition as the other groups. Control group: 1 h of ischemia followed by 4 h of reperfusion. The vehicle group was the same as the control, but they were given the vehicle intraperitoneally (1 ml/kg of 0.9 % NaCl) for 7 days before the ischemia. The treatment group as the control group, but they were given tocilizumab (8 mg/ kg) intraperitoneally for 7 days before ischemia. Results: control group, inducing ischemia/reperfusion increased infarction size considerably (p<0.001), when comparison to the control and vehicle groups, tocilizumab at dose (8 mg/kg) showed a significantly (p<0.001) smaller infraction area. Conclusions: In a cerebral ischemia/reperfusion, a reduction in infarction area in injected with Tocilizumab medication was considered neuroprotective for cerebral ischemia/reperfusion.