Curcumin inhibits UV irradiation-induced oxidative stress and apoptotic biochemical changes in human epidermoid carcinoma A431 cells

✍ Scribed by Wen-Hsiung Chan; Chih-Ching Wu; Jau-Song Yu

• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 317 KB
• Volume: 90
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.10638

✦ Synopsis

Abstract

Ultraviolet (UV) light is a strong apoptotic trigger that induces caspase‐dependent biochemical changes in cells. Previously we showed that UV irradiation can activate caspase‐3, and the subsequent cleavage and activation of p21^Cdc42/Rac^‐activated kinase 2 (PAK2) in human epidermoid carcinoma A431 cells. In this study we demonstrate that curcumin (Cur), the yellow pigment of Curcuma longa with known anti‐oxidant and anti‐inflammatory properties, can prevent UV irradiation‐induced apoptotic changes, including c‐Jun N‐terminal kinase (JNK) activation, loss of mitochondrial membrane potential (MMP), mitochondrial release of cytochrome C, caspase‐3 activation, and cleavage/activation of PAK2 in A431 cells. Flow cytometric analysis using the cell permeable dye 2′,7′‐dichlorofluorescin diacetate (DCF‐DA) as an indicator of reactive oxygen species (ROS) generation revealed that the increase in intracellular oxidative stress caused by UV irradiation could be abolished by Cur. In addition, we found that SP600125, a JNK‐specific inhibitor, reduced UV irradiation‐induced JNK activation as well as caspase‐3 activation, indicating that JNK activity is required for UV irradiation‐induced caspase activation. Collectively, our results demonstrate that Cur significantly attenuates UV irradiation‐induced ROS formation, and suggest that ROS triggers JNK activation, which in turn causes MMP change, cytochrome C release, caspase activation, and subsequent apoptotic biochemical changes. J. Cell. Biochem. 90: 327–338, 2003. © 2003 Wiley‐Liss, Inc.