This paper is part of the Special Issue in Commemoration of the 70th birthday of Dr. David R. Bickers.
Silibinin Is a Potent Sensitizer of UVA Radiation-induced Oxidative Stress and Apoptosis in Human Keratinocyte HaCaT Cells†
Article first published online: 10 JAN 2012
© 2012 Wiley Periodicals, Inc. Photochemistry and Photobiology © 2012 The American Society of Photobiology
Photochemistry and Photobiology
Volume 88, Issue 5, pages 1135–1140, September/October 2012
How to Cite
Narayanapillai, S., Agarwal, C., Tilley, C. and Agarwal, R. (2012), Silibinin Is a Potent Sensitizer of UVA Radiation-induced Oxidative Stress and Apoptosis in Human Keratinocyte HaCaT Cells. Photochemistry and Photobiology, 88: 1135–1140. doi: 10.1111/j.1751-1097.2011.01050.x
- Issue published online: 5 SEP 2012
- Article first published online: 10 JAN 2012
- Accepted manuscript online: 25 NOV 2011 12:13PM EST
- Received 16 November 2011, accepted 20 November 2011
UVA radiation (315–400 nm), which constitutes ca 95% of the UV irradiation in natural sunlight reaching earth surface, is a major environmental risk factor associated with human skin cancer pathogenesis. UVA is an oxidizing agent that causes significant damage to cellular components through the release of reactive oxygen species (ROS) and leads to photoaging and photocarcinogenesis. Here we investigate the effect of silibinin, the flavonolignan from Silybum marianum, on UVA-induced ROS and cell death in human keratinocyte cell line HaCaT. In addition, the effect of silibinin on UVA-induced intracellular ROS-mediated endoplasmic reticulum (ER) stress was also analyzed. UVA irradiation resulted in ROS production and apoptosis in HaCaT cells in a dose-dependent manner, and the ROS levels and apoptotic index were found to be elevated significantly when the cells were treated with 75 μmsilibinin for 2 h before UVA exposure. When the cells were pretreated with 10 mmN-acetyl cysteine, the enhancement of UVA-induced apoptosis by silibinin was compromised. Furthermore, we found that silibinin enhances ER stress-mediated apoptosis in HaCaT cells by increasing the expression of CHOP protein. These results suggest that silibinin may be beneficial in the removal of UVA-damaged cells and the prevention of skin cancer.