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首页> 外文期刊>International Journal of Preventive Medicine >The Effect of Pioglitazone on the Alzheimer's Disease-Induced Apoptosis in Human Umbilical Vein Endothelial Cells
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The Effect of Pioglitazone on the Alzheimer's Disease-Induced Apoptosis in Human Umbilical Vein Endothelial Cells

机译：吡格列酮对阿尔茨海默氏病诱导的人脐静脉内皮细胞凋亡的影响

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Background: Alzheimer's disease (AD) is a progressive neurodegenerative disease and nowadays the role of endothelial cell (EC) injury has been proposed in pathological process in AD. Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist has anti-inflammatory properties through activation in glial cells and improves vascular function and prevent atherosclerotic disease progression. The aim of this study is evaluation of pioglitazone effects as a drug of PPAR-γ agonist on endothelial apoptosis induced by sera from AD patients. Methods: Human umbilical vein endothelial cells (HUVECs) were treated with sera from AD patients ( n = 10) and sera from controls ( n = 10). Apoptosis was identified by annexin V-propidium iodide staining and cell death detection kit. Apoptosis was evaluated after and before adding of 10 μM pioglitazone on EC. Nitrite (NO2-) levels were determined in the culture supernatants. Results: Induced apoptosis by the serum of patients was inhibited markedly when pioglitazone used before treating HUVECs with the sera of AD. Also, the measurement of nitrite concentration showed significantly greater levels of dissolved NO2/NO3 metabolite in the culture media of HUVECs treated by sera of AD patients ( P 0.05), while the rate of nitric oxide significantly decreased when pioglitazone exists in culture media. Conclusion: Further studies are justified to investigate the novel role of the PPARs in the prevention of the neuronal and endothelial damage in neurological disorder and present a new therapeutic approach for Alzheimer's patients.
机译：背景：阿尔茨海默氏病（AD）是一种进行性神经退行性疾病，如今，人们已经提出了内皮细胞（EC）损伤在AD病理过程中的作用。过氧化物酶体增殖物激活受体-γ（PPAR-γ）激动剂通过激活神经胶质细胞具有抗炎特性，并改善血管功能并防止动脉粥样硬化疾病的进展。这项研究的目的是评估吡格列酮作为PPAR-γ激动剂对AD患者血清诱导的内皮细胞凋亡的作用。方法：用AD患者的血清（n = 10）和对照患者的血清（n = 10）处理人脐静脉内皮细胞（HUVEC）。通过膜联蛋白V-碘化丙啶染色和细胞死亡检测试剂盒鉴定凋亡。在EC上添加10μM吡格列酮之后和之前评估细胞凋亡。测定培养上清液中的亚硝酸盐（NO2-）水平。结果：在用AD血清治疗HUVECs之前使用吡格列酮明显抑制了患者血清诱导的细胞凋亡。此外，亚硝酸盐浓度的测量结果显示，AD患者血清治疗的HUVEC培养基中溶解的NO2 / NO3代谢产物水平显着升高（P <0.05），而当吡格列酮存在于培养基中时，一氧化氮的比率显着降低。结论：有必要进行进一步的研究以研究PPAR在预防神经系统疾病中神经元和内皮损伤中的新作用，并为阿尔茨海默氏病患者提供一种新的治疗方法。

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