Pyrogallol-induced endothelial cell death is related to GSH depletion rather than ROS level changes.
Pyrogallol (PG) as a polyphenol compound induces apoptosis in several types of cells. Here, we evaluated the effects of PG on endothelial cells (ECs), especially calf pulmonary artery endothelial cells (CPAEC) in relation to the cell growth, ROS and glutathione (GSH) levels. PG dose-dependently inhibited the growth of CPAEC and human umbilical vein endothelial cells (HUVEC) at 24 h. PG also induced apoptosis in CPAEC, which was accompanied by the loss of mitochondrial membrane potential (MMP; DeltaPsim). PG decreased ROS level including O2*- and PG dose-dependently increased GSH depleted cell number in both EC types. N-acetyl-cysteine (NAC; a well-known antioxidant) increased ROS levels in PG-treated CPAEC with the prevention of cell death and GSH depletion. In conclusion, PG inhibited the growth of ECs, especially CPAEC via apoptosis. PG-induced EC death was related to GSH depletion rather than ROS level changes.
Han
Yong Hwan
YH
Department of Physiology, Medical School, Centers for Healthcare Technology Development Institute for Medical Sciences Chonbuk National University, Jeonju, Republic of Korea.
Moon
Hwa Jin
HJ
You
Bo Ra
BR
Kim
Sung Zoo
SZ
Kim
Suhn Hee
SH
Park
Woo Hyun
WH
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D017209:Apoptosis; D002417:Cattle; D049109:Cell Proliferation; D042783:Endothelial Cells / Q000187:drug effects*; D005786:Gene Expression Regulation; D005978:Glutathione / Q000378:metabolism*; D006801:Humans; D008564:Membrane Potentials; D008928:Mitochondria / Q000378:metabolism; D010100:Oxygen / Q000737:chemistry; D011748:Pyrogallol / Q000494:pharmacology*; D017382:Reactive Oxygen Species; D014471:Umbilical Veins / Q000166:cytology
D000975:Antioxidants; D017382:Reactive Oxygen Species; D011748:Pyrogallol; D005978:Glutathione; D010100:Oxygen