J Cancer Sci Ther 2009 1: 078-082. doi:10.4172/1948-5956.1000012
Tatsuo Ishikawa, Jun Ishibashi, Kikuji Yamashita, Shine-Od Dalkhsuren, Kaori Sumida, Takahumi Masui and Seiichiro Kitamura
Department of Oral and Maxillofacial Anatomy, Medical Science for Oral and Maxillofacial Regeneration, Graduate School of Health Biosciences, University of Tokushima, 3-18-15 Kuramoto, Tokushima, 770-8504 Japan
Background: We developed a cell culture CO2 incubator and a mice rack that can continuously irradiate cells or murine with Far Infrared Ray. Our goal is to make clear the non-thermal effect of FIR on HepG2 with these instruments morphologically.
Methods: By using them, in vitro , we examined the proliferation of cultured HepG2 cells with hematocytometer, BrdU assay, WST-1 assay, HE staining, Toluidine blue staining and microarray studies. And in vivo, we measured the tumors, observed the sections by IHC, DAPI staining with light microscopes and performed microarray studies.
Results: Proliferation of HepG2 cells were suppressed (e.g., cell count declined by 34% after 10 days of Far Infrared Ray irradiation), tumor volumes reduced by 86% after 30 days of Far Infrared Ray irradiation, mRNA of Vascular Endothelial Growth Factor (VEGF) decreased by 48%, vascular area in cross sections from the tumors decreased 60% compared with the control. More frequent properties in apoptosis were observed by TUNEL and DAPI staining in FIR-treated groups. Body weight of mice increased compared with the control. Oxydation and Reduction (Redox) reactions by H+ (proton and electron)/O2- (a kind of Reactive Oxygen Species (ROS)) were induced by FIR.
Conclusions: These results clarified that Far Infrared Rays inhibited the proliferation of HepG2 at non-thermal circumstances (at 25±0.5, 37±0.5°C). Far Infrared Rays will serve as a tool against diseases induced by HepG2.