Background: Oxidized low-density lipoprotein (ox-LDL) has an important role in the genesis of coronary atherosclerosis. Lectin-like ox-LDL receptor 1 (OLR1) contributes to the uptake and internalization of ox-LDL. Genetic polymorphisms have been associated with coronary artery disease (CAD). Here we explore the association of plasma levels of ox-LDL and 3′ UTR OLR1 (rs1050286) SNP with CAD risk and inhospital adverse outcomes. Methods: A case-control study enrolled 192 patients with ST-segment elevation myocardial infarction (STEMI), 100 patients with unstable angina, and 100 healthy controls. Baseline, clinical characteristics, and risk scores of the patients were determined. Plasma ox-LDL and other biochemical variables were measured. All subjects are genotyped for OLR1 (rs1050286) by RT-PCR with TaqMan SNP genotyping assay. Results: Plasma ox-LDL was higher with enhanced sensitivity and specificity in identifying patients with STEMI and was found as a significant independent risk factor for CAD in those two groups. Levels of ox-LDL were increased with increasing poor prognostic factors in STEMI patients that are associated with an increased incidence of some adverse events and in-hospital mortality. Elevated STEMI risk was associated with T allele of OLR1 (rs1050286) (odds ratio of 4.9, 95% CI: 2.6-9.4, p< 0.001). STEMI patients who have T allele exhibited higher risk scores, coronary multivessel narrowing, and elevated incidence of in-hospital major adverse clinical events. Conclusions: These results suggest that plasma ox-LDL, as well as T allele of ORL-1 (rs1050286), is associated with the increased risk for developing STEMI and the associated adverse clinical outcomes.
Background: Liraglutide is an incretin mimetic agent that approved recently in type-2 diabetes. The use of vitamin D was reported to be associated with an improvement in diabetic neuropathy. The aim of the study: Evaluation of the effect of liraglutide and vitamin D each alone and in combination with each other on diabetic neuropathy induced by streptozotocin in rats. Materials and Methods: Five groups of Wistar rats were used in the experiment. Diabetic neuropathy was induced in groups 2, 3, 4, and 5 using a single intraperitoneal(i.p.) injection of streptozotocin(STZ) in a dose of 60 mg/kg. The third, fourth, and fifth groups were treated for 4 weeks with liraglutide (0.8 mg/kg), vitamin D (12 µg/kg), and combination of the 2 drugs, respectively. Then the behavioral tests were done (hot plate, tail-flick, paw withdrawal pressure, and the rotarod tests). Blood samples were used for assessment of blood glucose, tumor necrosis factor-α (TNF-α) and interleukin-Iβ(IL-Iβ).Malondialdehyde(MDA) and glutathione (GSH)were measured in the sciatic nerve homogenate. Results: Liraglutide caused significant improvement in the behavioral tests of the diabetic rats with a significant reduction in blood glucose, TNF-α, IL-1β, and malondialdehyde. Vitamin D caused mild improvement in the behavioral tests, inflammatory and oxidative stress markers. The combined use of liraglutide with vitamin D caused more improvement in diabetic neuropathy tests, inflammatory and oxidative stress markers. Conclusion: Liraglutide has a moderate neuroprotective, anti-inflammatory, and antioxidant effects in cases of streptozotocin-induced diabetic neuropathy which are enhanced by the addition of vitamin D.
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