Our results demonstrated that expression of IL-6 and COX-2 were remarkably up-regulated in peripheral blood of DMCI patients compared with that in normal control group.
These results suggest that diabetes induces hypereactivity of the rabbit renal artery to BNP by mechanisms that at least include (1) a reduced vasoconstrictor influence of arachidonic acid metabolites via cyclooxygenase 2, which is not related with changes in thromboxane A<sub>2</sub> and prostacyclin release from the arterial wall and (2) a selectively increased modulatory activity of K<sub>ATP</sub> and endothelial IK<sub>Ca</sub> channels.
Combination COX-2 inhibitor and metformin attenuate rate of joint replacement in osteoarthritis with diabetes: A nationwide, retrospective, matched-cohort study in Taiwan.
The intensities of COX-2 staining of coronary arterioles and COX-2 protein levels in myocardium were higher in diabetes than nondiabetes at baseline (p < 0.05).
After CPB, bradykinin-induced relaxation response of the ND and DM arterioles was inhibited in the presence of the specific COX-2 inhibitor NS398, but this effect was more pronounced in the diabetic patients (P < 0.05).
These data suggest that <i>1</i>) KO of COX2 in podocytes does not ameliorate diabetic kidney disease in Akita mice, and <i>2</i>) some basal level of podocyte COX2 expression in podocytes is necessary to attenuate the adverse effects of diabetes on glomerular filtration barrier function.
The products of COX-2 and LOX activities have been implicated in cytokine-mediated damage of beta-cells, so selective inhibitors of these enzymes would be expected to have a dual protective role in diabetes: they would minimize beta-cell dysfunction while maintaining insulin secretion through enhancing endogenous arachidonic acid levels.
In this study we evaluated whether diabetic conditions in vitro, such as high-glucose (HG) culture or AGE, or in vivo in animal models of diabetes can induce PTGS2 expression and activity in pancreatic islets.
This review will explore experimental and clinical evidence that VEGF, COX-2 and NO promote retinal pathology in diabetes and other ischemic-induced retinopathies.