SB203580 enhances the RV-induced loss of mitochondrial membrane potential and apoptosis in A549 cells

Hai-yang Li; Cai-ping Zhuang; Xiao-ping Wang; Tong-sheng Chen

doi:10.1117/12.904961

15 February 2012 SB203580 enhances the RV-induced loss of mitochondrial membrane potential and apoptosis in A549 cells

Hai-yang Li, Cai-ping Zhuang, Xiao-ping Wang, Tong-sheng Chen

Proceedings Volume 8224, Biophotonics and Immune Responses VII; 82240L (2012) https://doi.org/10.1117/12.904961
Event: SPIE BiOS, 2012, San Francisco, California, United States

Abstract

Resveratrol (RV), a naturally occurring phytoalexin, is known to possess a wide spectrum of chemopreventive and chemotherapeutic effects in various stages of human tumors. p38, a member of the mitogen-activated protein kinase (MAPK) superfamily, is always activated by some extracellular stimulus to regulate many cellular signal transduction pathways, such as apoptosis, proliferation, and inflammation and so on. In this report, we assessed the effect of SB203580, a specific inhibitor of p38 MAPK signaling pathway, on the RV-induced apoptosis in human lung adenocarcinoma (A549) cells. CCK-8 assay showed that pretreatment with SB203580 significantly enhanced the cytotoxicity of RV, which was further verified by analyzing the phosphatidylserine externalization using flow cytometry. In order to further confirm whether SB203580 accelerated apoptosis via the intrinsic apoptosis pathway, we analyzed the dysfunction of mitochondrial membrane potential (Δψ_m) of cells stained with rhodamine 123 by using flow cytometry after treatment with RV in the absence and presence of SB203580. Our data for the first time reported that p38 inhibitor SB203580 enhanced the RV-induced apoptosis via a mitochondrial pathway.

Citation Download Citation

Hai-yang Li, Cai-ping Zhuang, Xiao-ping Wang, and Tong-sheng Chen "SB203580 enhances the RV-induced loss of mitochondrial membrane potential and apoptosis in A549 cells", Proc. SPIE 8224, Biophotonics and Immune Responses VII, 82240L (15 February 2012); https://doi.org/10.1117/12.904961

ACCESS THE FULL ARTICLE

INSTITUTIONAL
Select your institution to access the SPIE Digital Library.

SELECT YOUR INSTITUTION

PERSONAL
Sign in with your SPIE account to access your personal subscriptions or to use specific features such as save to my library, sign up for alerts, save searches, etc.

PERSONAL SIGN IN

No SPIE Account? Create one

PURCHASE THIS CONTENT

SUBSCRIBE TO DIGITAL LIBRARY

50 downloads per 1-year subscription

Members: $195

Non-members: $335 ADD TO CART

25 downloads per 1 - year subscription

Members: $145

Non-members: $250 ADD TO CART

PURCHASE SINGLE ARTICLE

Includes PDF, HTML & Video, when available