Comparing Anti-apoptotic Effects of Peroxisome Proliferator-Activated Receptor-Gamma and Angiotensin-Converting Enzyme Inhibitors using Human Umbilical Vein Endothelial Cells Exposed to Sera from Patients with Alzheimer's Disease and Healthy Controls

Alzheimer''s disease (AD)، the most frequent progressive neurodegenerative disorder، is associated with endothelial cell dysfunction. It has been presented that peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists can attenuate neurodegeneration of experimental autoimmune encephalomyelitis (EAE) and improve vascular function. On the other hand، angiotensin-converting enzyme inhibitors (ACE-I) has beneficial effects on endothelial dysfunction and endothelial surveillance. This study aimed to compare the beneficial effects of PPAR-gamma and ACE-I on human umbilical vein endothelial cells (HUVECs) treated with sera from patients with Alzheimer''s disease or healthy controls.

10 patients with Alzheimer''s disease and 10 healthy individuals were arranged in case and control groups، respectively. Apoptosis was identified after and before adding pioglitazone and enalapril on endothelial cells by annexin V‐propidium iodide staining and cell-death detection kit. Although، nitrite levels were diminished when the sera exposed to both drugs treated endothelial cells but this difference between them was not significant.

Pioglitazone and enalapril could attenuate apoptosis rate significantly before treating with sera from patients with Alzheimer''s disease but the reduction rate was more when pioglitazone added to the media. Also، nitrite concentration showed significantly greater levels of dissolved NO2/NO3 metabolite in the culture media of endothelial cells treated by sera of patients with Alzheimer''s disease (P < 0. 05)، while the rate of nitric oxide significantly decreased when both drugs were presented in culture media.

Overally، apoptosis rate reduced more when PPAR agonist was added than ACE-I drugs. It seems that poiglitazone stimulate more anti-apoptotic mechanisms in Alzheimer''s disease.