enalapril protects endothelial cells against induced apoptosis in alzheimer's disease in vitro

normal 0 false false false en-us x-none ar-sa background: alzheimer's disease (ad) is a progressive neurodegenerative disease in which endothelial cell (ec) can be affected. in brain, functional changes in ecs contribute to reductions in resting blood flow. furthermore, angiotensin-converting enzyme inhibitors (ace-i) have beneficial effects on endothelial dysfunction. this is the first study that presents direct experimental evidence associating endothelial apoptosis as a basis of ad pathogenesis and response to an ace-i therapy. materials and methods: human umbilical vein ecs (huvecs) were treated with sera from ad patients and sera from healthy volunteers (each group, n = 10). apoptosis was determined by annexin v–propidium iodide staining and cell death detection kit. the effect of 50 µm enalapril on endothelial apoptosis was assessed. nitrite (no 2 − ) levels were determined in the culture supernatants. result s: enalapril suppressed the induction of apoptosis by the serum of patients only when used before treating huvecs with the sera of ad. mean ± sd of apoptosis induction in the control group was 6.7 ± 3.69; in the group treated with sera of ad for 24 h was 47.78 ± 0.65; in the group wherein sera from ad was added (pretreatment) after exposure of huvecs by 50 µm enalapril for 24 h was 26.6 ± 2.63; and in the group wherein huvecs were exposed in the sera of ad for 24 h and then 50 µm enalapril was added to these cells for another 24 h (post-treatment) was 56.87 ± 5.51. also, the mean ± sd of no 2 − concentration showed significantly greater levels of dissolved no 2 /no 3 metabolite in the culture media of untreated huvecs by enalapril (1.03 ± 0.06) as compared with control (0.26 ± 0.13; p < 0.05), while the rate of nitric oxide (no) significantly decreased when enalapril was presented in culture both in the pretreatment (0.07 ± 0.003) and in the post-treatment group (0.06 ± 0.005; p < 0.05). conclusion: it could be concluded that ec treated with sera from ad patients activates apoptosis in huvecs; this effect was reversed by enalapril pretreatment. this can be proposed as a therapeutic approach for alzheimer`s patients.