Chemopreventive effects of β-caryophyllene against cigarette smoke damage in upper airway cells

Exposure to cigarette smoke induces damages in different organs and tissues, and high incidence of precancerous lesions and malignancies particularly at upper respiratory tract.1 Increasing levels of reactive oxygen species (ROS) and the activation of STAT3 pathway seems to be involved in smoke injury and oncogenic proliferation of damaged cells.1 In order to find new strategies for preventing cancer development in smokers, in present study we evaluated the ability of the natural sesquiterpene β-caryophyllene (CRY) to inhibit smoke damage in human epithelial bronchial upper airway (BEAS-2B) cells, by studying the inhibition of STAT3-phosphorylation, pro-oxidant damage and oncogenic proliferation induced by a condensed sample of cigarette smoke (CSC), according to previous methods.2,3 In our experiments, CSC (25-150 g/ml) strongly increased the levels of both phosphorylated STAT3 and intracellular ROS, and the cell migration capacity. CRY (1-10 g/ml) significantly reduced the activation of STAT3 pathway and the pro-oxidant effects of CSC (75 μg/ml). Furthermore, a remarkable inhibition of CSC-induced cell migration was highlighted, so suggesting a possible interference of CRY with metastatic ability of damaged cells. Data obtained highlight interesting protective properties of CRY and encourage further studies in order to evaluate its possible use as a chemopreventive agent against smoke damage. References 1. Wu et al. (2014). Free Rad. Biol. Med. 69, 208–218. 2. Chichiarelli et al. (2010). Arch Biochem Biophys 494, 178-193. 3. Duan et al. (2013). Plos One 8, e57941.