Anti-apoptotic effects of curcumin on photosensitized human epidermal carcinoma A431 cells

✍ Scribed by Wen-Hsiung Chan; Hsin-Jung Wu

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 419 KB
• Volume: 92
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.20059

✦ Synopsis

Abstract

Photodynamic treatment (PDT) can elicit a diverse range of cellular responses, including apoptotic cell death. Previously, we showed that PDT stimulates caspase‐3 activation and subsequent cleavage and activation of p21‐activated kinase 2 (PAK2) in human epidermal carcinoma A431 cells. Curcumin, the yellow pigment of Curcuma longa, is known to have anti‐oxidant and anti‐inflammatory properties. In the present study, using Rose Bengal (RB) as the photosensitizer, we investigated the effect of curcumin on PDT‐induced apoptotic events in human epidermal carcinoma A431 cells. We report that curcumin prevented PDT‐induced JNK activation, mitochondrial release of cytochrome c, caspase‐3 activation, and cleavage of PAK2. Using the cell permeable dye DCF‐DA as an indicator of reactive oxygen species (ROS) generation, we found that both curcumin and ROS scavengers (i.e., l‐histidine, a‐tocopherol, mannitol) abolished PDT‐stimulated intracellular oxidative stress. Moreover, all these PDT‐induced apoptotic changes in cells could be blocked by singlet oxygen scavengers (i.e., l‐histidine, a‐tocopherol), but were not affected by the hydroxyl radical scavenger mannitol. In addition, we found that SP600125, a JNK‐specific inhibitor, reduced PDT‐induced JNK activation as well as caspase‐3 activation, indicating that JNK activity is required for PDT‐induced caspase activation. Collectively, these results demonstrate that singlet oxygen triggers JNK activation, cytochrome c release, caspase activation and subsequent apoptotic biochemical changes during PDT and show that curcumin is a potent inhibitor for this process. © 2004 Wiley‐Liss, Inc.