Premium
Curcumin Induces Autophagy to Protect Vascular Endothelial Cell Survival from Oxidative Stress Damage
Author(s) -
Li XueJun,
Han Jing
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.lb613
Subject(s) - curcumin , autophagy , oxidative stress , microbiology and biotechnology , umbilical vein , chemistry , gene knockdown , foxo1 , viability assay , pharmacology , apoptosis , cancer research , biology , biochemistry , in vitro , protein kinase b
Our study first proposed that curcumin could protect human endothelial cells from the damage caused by oxidative stress via autophagy. Furthermore, our results revealed that curcumin causes some novel cellular mechanisms that promote autophagy as a protective effect. Pretreatment with curcumin remarkably improves the survival of human umbilical vein endothelial cells (HUVECs) from H 2 O 2 ‐induced viability loss. Exposed to H 2 O 2 , curcumin‐treated HUVECs upregulate the level of microtubule‐associated protein 1 light chain 3‐II (LC3‐II), the number of autophagosomes, and the degradation of p62. Curcumin can also reverse FOXO1 (a mediator of autophagy) nuclear localization along with causing an elevated level of cytoplasmic acetylation of FOXO1 and the interaction of acetylated FOXO1 and ATG7, under the circumstance of oxidative stress. Additionally, knockdown of FOXO1 by shRNA inhibits not only the protective effects that curcumin induced, but the autophagic process, from the quantity of LC3‐II to the expression of RAB7. These data uncover a brand new protective mechanism involving FOXO1 as having a critical role in regulating autophagy in HUVECs, and suggest a novel role for curcumin in inducing a beneficial form of autophagy in HUVECs, which may be a potential multitargeted therapeutic avenue for the treatment of oxidative stress‐related cardiovascular diseases. This work was supported by the National Natural Science Foundation of China.