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过氧化物酶体增殖物激活受体-γ 激动剂吡格列酮可防止大鼠骨髓内皮祖细胞凋亡。

PPAR-γ agonist pioglitazone prevents apoptosis of endothelial progenitor cells from rat bone marrow.

机构信息

The Second Department of Endocrinology, Henan Provincial People's Hospital, Zhengzhou Henan Province, China.

出版信息

Cell Biol Int. 2013 May;37(5):430-5. doi: 10.1002/cbin.10046. Epub 2013 Mar 18.

DOI:10.1002/cbin.10046
PMID:23504801
Abstract

Selective peroxisome proliferator-activated receptor-γ (PPAR-γ) agonist affects the functions of endothelial progenitor cells (EPCs). This study explores the effect of selective PPAR-γ agonist, pioglitazone, on EPC apoptosis. The cells were cultured and identified via the double staining method in a medium containing different concentrations of pioglitazone. EPC apoptosis was detected by flow cytometry. On Day 7, EPCs engulfed DiL-ac-LDL and FITC-UEA-1, and showed yellow fluorescence in a laser-scanning confocal microscope. EPC apoptosis inhibition was maximal at 50 µmol/L. The ability of pioglitazone to prevent EPC apoptosis may be mediated by the PI3K/Akt signal pathway. The use of thiazolidine two ketone (TZD) to reduce EPC apoptosis may have some potential in treating vascular diseases.

摘要

选择性过氧化物酶体增殖物激活受体-γ(PPAR-γ)激动剂影响内皮祖细胞(EPCs)的功能。本研究探讨了选择性 PPAR-γ 激动剂吡格列酮对 EPC 细胞凋亡的影响。采用不同浓度吡格列酮的培养基,通过双染色法培养和鉴定细胞。通过流式细胞术检测 EPC 细胞凋亡。在第 7 天,EPCs 吞噬 DiL-ac-LDL 和 FITC-UEA-1,在激光共聚焦显微镜下呈现黄色荧光。50μmol/L 时 EPC 细胞凋亡抑制作用最大。吡格列酮预防 EPC 细胞凋亡的能力可能是通过 PI3K/Akt 信号通路介导的。使用噻唑烷二酮(TZD)减少 EPC 细胞凋亡可能在治疗血管疾病方面具有一定的潜力。

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