A butyrolactone derivative suppressed lipopolysaccharide-induced autophagic injury through inhibiting the autoregulatory loop of p8 and p53 in vascular endothelial cells

Article ID	Journal	Published Year	Pages	File Type
1984095	The International Journal of Biochemistry & Cell Biology	2012	9 Pages	PDF

Abstract

âº 3BDO inhibited LPS-induced autophagic injury in HUVECs. âº 3BDO depressed LPS-induced increase of p8 and p53 levels and inhibited LPS-induced nuclear translocation of p53. âº Ros and p8 were involved in LPS-induced HUVEC autophagy. âº Knockdown of p8 inhibited the p53 protein level increase, the translocation of p53 into nuclei and the ROS level increase induced by LPS in HUVECs.

Keywords

p53 NAC HUVECS FGF-2 PVDF JC-1 LC3-II VEC FBS LPS LC3-I PBS MMP 2′,7′-dichlorodihydrofluorescein 5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimidazolylcarbocyanine iodide BSA DMSO N-acetylcysteine RNA interference Small interfering RNA RNAi ROS siRNA bovine serum albumin Autophagy Dimethyl sulfoxide fetal bovine serum vascular endothelial cell Human umbilical vein endothelial cells Vascular endothelial cells fibroblast growth factor-2 lipopolysaccharide Phosphate-buffered saline Mitochondrial membrane potential Polyvinylidene fluoride optical density Reactive oxygen species