焦性没食子酸诱导小牛肺动脉内皮细胞通过半胱天冬酶依赖性细胞凋亡和 GSH 耗竭而死亡。
Pyrogallol-induced calf pulmonary arterial endothelial cell death via caspase-dependent apoptosis and GSH depletion.
机构信息
Department of Physiology, Medical School, Institute for Medical Sciences, Chonbuk National University, JeonJu 561-180, Republic of Korea.
出版信息
Food Chem Toxicol. 2010 Feb;48(2):558-63. doi: 10.1016/j.fct.2009.11.032. Epub 2009 Nov 12.
Pyrogallol (PG) as a polyphenol induces apoptosis in cells. Here, we evaluated the effects of PG on the growth and death of endothelial cells (ECs). PG dose-dependently inhibited the growth of calf pulmonary artery endothelial cells (CPAEC) and human umbilical vein endothelial cells (HUVEC). PG also induced apoptosis in both cells accompanied by the loss of mitochondrial membrane potential (DeltaPsi(m)). CPAEC were more sensitive to PG than HUVEC concerning cell growth and death. Caspase inhibitors (pan-caspase, caspase-3, -8 or -9 inhibitor) did not affect the growth inhibition of CPAEC by PG. However, pan-caspase inhibitor (Z-VAD) significantly reduced apoptosis and the loss of DeltaPsi(m) in PG-treated CPAEC. PG reduced ROS level and increased GSH depleted cell numbers in CPAEC. While Z-VAD increased ROS levels in PG-treated CPAEC, it decreased GSH depleted cell numbers. In conclusion, PG inhibited the growth of ECs, especially CPAEC via caspase-dependent apoptosis and GSH depletion.
焦性没食子酸（PG）作为一种多酚诱导细胞凋亡。在这里，我们评估了 PG 对内皮细胞（EC）生长和死亡的影响。PG 呈剂量依赖性地抑制小牛肺动脉内皮细胞（CPAEC）和人脐静脉内皮细胞（HUVEC）的生长。PG 还诱导这两种细胞凋亡，伴随着线粒体膜电位（DeltaPsi(m)）的丧失。CPAEC 比 HUVEC 对 PG 更敏感，表现在细胞生长和死亡方面。半胱天冬酶抑制剂（pan-caspase、caspase-3、-8 或 -9 抑制剂）不影响 PG 对 CPAEC 生长的抑制作用。然而，pan-caspase 抑制剂（Z-VAD）显著减少了 PG 处理的 CPAEC 中的细胞凋亡和 DeltaPsi(m) 的丧失。PG 降低了 CPAEC 中的 ROS 水平并增加了 GSH 耗竭细胞的数量。虽然 Z-VAD 增加了 PG 处理的 CPAEC 中的 ROS 水平，但它降低了 GSH 耗竭细胞的数量。总之，PG 通过半胱天冬酶依赖性细胞凋亡和 GSH 耗竭抑制 EC 的生长，特别是 CPAEC。
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