European Journal of Molecular & Clinical Medicine

Background: Stroke was commonly identified as a neurologically impairment that occur in central nervous system on vascular basis as Acute focal injury. Statin (HMG-CoA reductase Inhibitor), clinical trials in many large scaled shown that in primary and secondary CVD the used of statin was declined rates of (CV). Human Lipoprotein Lipase (LPL) gene coding was place in short arm of chromosome in the p22 region of the same Chromosome and has nine introns and ten axons. Aim: The aim of the study is to find out effect of LPL gene polymorphism of response to atorvastatin treatment in patients with ischemic stroke. Patients and methods: Samples was Picking up from patients’ admission to at Middle Euphrates Center for Neurological Sciences in the main hospital for measurement of the lipid profile, molecular analysis study of genotyping and measurement of human lipoprotein lipase by ELISA technique. Result: There is good response to treatment and the response consider statistically significant, the best group response to treatment was homozygous mutation then Heterozygous mutation and the less group response was Homozygous normal, wild. Conclusion: The effect of drug on serum biomarker not affected by age except HDL (best result in age<60yr), and not affected by gender and weight state, while in consider to smoking and Hypertension TG (best response in non-smoker, hypertensive) and VLDL (best response in smoker, hypertensive) affected and in diabetic state the Cholesterol and TG affected on response (the best result in non-diabetic). Heterozygous mutation most distributed then homozygous normal and the less distributed was homozygous mutation.

Background: Restriction of cerebral blood flow can disturb cellular homeostasis due to insufficient oxygen and nutrient delivery. However, the re-establishment of cerebral blood flow can aggravate the impairment of ischemic brain tissue contributing to a series of oxidative,  inflammatory events resulting in cerebral ischemia-reperfusion (CI/R) injury, which eventually results in neuronal death and neurological disability. Method: An experimental model of 30 Sprague-Dawley rats were randomly allocated to five groups, sham group, I/R group, I/R+(DMSO as a vehicle),I/R+ intraperitoneal (i.p) Empagliflozin 5mg/kg 1 hour before induction of BCCAO, and I/R+intraperitoneal Empagliflozin 10mg/kg 1hour before induction of BCCAO. The brain tissue levels of IL-1β, ICAM-1, and F2-isoprostane were measured in each group in our study. Results: The two doses of (5mg/kg and 10mg/kg) Empagliflozin were significantly reduced the brain tissue level of IL-1β, ICAM-1, and F2-isoprostane as compared to I/R and I/R+vehicle groups.Conclusions: From the results above we concluded that Empagliflozin has a neuroprotective effect seeing that it’s antiinflammatory and anti-oxidant activity.